Egs Guidelines 4 English (Unlocked by WWW - Freemypdf.com)

AND
TERMINOLOGY
FOR
GUIDELINES
GLAUCOMA
4th Edition
www.eugs.org
ISBN 978-88-98320-05-9
Piazza Guido Rossa 8r

17100 Savona - Italy
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Printed in EU
June 2014
Copyright © 2014 European Glaucoma Society
No parts of this text, illustrations, tables or flowcharts can be reproduced, copied, translated
or stored by any means including magnetic, electronic or multimedia formats without written
permission of the European Glaucoma Society.
AND
TERMINOLOGY
FOR
GUIDELINES
GLAUCOMA
4th Edition
www.eugs.org
Contents
Page
FOREWORD 6
INTRODUCTION CHAPTER 11
GLOSSARY 27
CHAPTER 1 - PATIENT EXAMINATION 31
1.1 Intraocular pressure (iop) and tonometry 33

1.2 Gonioscopy 39
1.3 Optic nerve head and retinal nerve fibre layer 48
1.4 Perimetry 58
CHAPTER 2 - CLASSIFICATION AND TERMINOLOGY 73
2.1 Primary congenital forms/childhood glaucomas 75

2.2 Primary open-angle glaucomas 79
2.3 Secondary Glaucomas 90
2.4 Primary Angle-Closure 100
2.5 Secondary Angle-Closure 114
CHAPTER 3 - TREATMENT PRINCIPLES AND OPTIONS 129
3.1 General Principles of Glaucoma Treatment 131

3.2 Target IOP and Quality of Life 134
3.3 Antiglaucoma Drugs 139
3.4 Adherence, Compliance and Persistence in Glaucoma 159
3.5 Laser Surgery 161
3.6 Incisional Surgery 169
3.7 Cataract and Glaucoma Surgery 176
INDEX 192
5
Foreword
It gives me pleasure to introduce the 4th edition of the EGS Guidelines. The Third
edition proved to be extremely successful, being translated into 7 languages with
over 70000 copies being distributed across Europe; it has been downloadable,
free, as a pdf file for the past 4 years. As one of the main objectives of the
European Glaucoma Society has been to both educate and standardize glaucoma
practice within the EU, these guidelines were structured so as to play their part.
Glaucoma is a living specialty, with new ideas on causation, mechanisms and

treatments constantly appearing. As a number of years have passed since the
publication of the last edition, changes in some if not all of these ideas would
be expected.
For this new edition of the guidelines a number of editorial teams were created,
each with responsibility for an area within the specialty; updating where necessary,
introducing new diagrams and Flowcharts and ensuring that references were up
to date. Each team had writers previously involved with the last edition as well
as newer and younger members being co-opted.
As soon as specific sections were completed they had further editorial comment
to ensure cross referencing and style continuity with other sections.
Overall guidance was the responsibility of Anders Heijl and Carlo Traverso.
Tribute must be made to the Task Force whose efforts made the timely publication
of the new edition possible.
Roger Hitchings
Chairman of the EGS Foundation
6
www.eugs.org
The Guidelines Writers The Guidelines The EGS Committees

and Contributors Task Force
CME and Certification
Augusto Azuara Blanco Luca Bagnasco Gordana Sunaric Mégevand
Luca Bagnasco Anders Heijl (Chair)
Alessandro Bagnis Carlo Enrico Traverso Carlo Enrico Traverso
Keith Barton (Co-chair)
Christoph Baudouin Augusto Azuara Blanco
Boel Bengtsson Alessandro Bagnis Delivery of Care
Alain Bron David Garway Heath Anton Hommer (Chair)
Francesca Cordeiro Michele Iester
Barbara Cvenkel Yves Lachkar EU Action
Philippe Denis Ingeborg Stalmans Thierry Zeyen (Chair)
Christoph Faschinger Gordana Sunaric Mégevand Carlo E. Traverso (Co-chair)
Panayiota Founti Fotis Topouzis
Stefano Gandolfi Anja Tuulonen Education
David Garway Heath Ananth Viswanathan John Thygesen (Chair)
Francisco Goñi Fotis Topouzis (Co-chair)
Franz Grehn
Anders Heijl The EGS Executive Glaucogene
Roger Hitchings
Committee Ananth Viswanathan (Chair)
Gábor Holló
Fotis Topouzis (Co-chair)
Tony Hommer
Carlo Enrico Traverso
Michele Iester
(President) Industry Liaison
Jost Jonas
Yves Lachkar Anja Tuulonen Roger Hitchings (Chair)
Giorgio Marchini (Vice President)
Frances Meier Gibbons Roger Hitchings Information Technology
Stefano Miglior (Past President) Ingeborg Stalmans (Chair)
Marta Misiuk-Hojło Anton Hommer Carlo E. Traverso (Co-chair)
Maria Musolino (Treasurer)
Jean Philippe Nordmann Barbara Cvenkel National Society Liaison
Norbert Pfeiffer Julian Garcia Feijoo Anders Heijl (Chair)
Luis Abegao Pinto David Garway Heath
Luca Rossetti Norbert Pfeiffer Program Planning
John Salmon Ingeborg Stalmans Fotis Topouzis (Chair)
Leo Schmetterer Ingeborg Stalmans (Co-chair)
Riccardo Scotto
Tarek Shaarawy The Board of the European Quality and Outcomes
Ingeborg Stalmans Glaucoma Society Foundation Anja Tuulonen (Chair)
Gordana Sunaric Mégevand Augusto Azuara Blanco
Ernst Tamm Roger Hitchings (Chair) (Co-chair)
John Thygesen Carlo E. Traverso (Vice Chair)
Fotis Topouzis Franz Grehn Scientific
Carlo Enrico Traverso Anders Heijl Franz Grehn (Chair)
Anja Tuulonen John Thygesen David Garway Heath
Ananth Viswanathan Fotis Topouzis (Co-chair)
Thierry Zeyen Thierry Zeyen
For Conflict of interest/Financial disclosure please see www.eugs.org/pdf/FinancialDisclosure.pdf
7
Introduction
Chapter
9
10
Introduction
Chapter
The aim of these Guidelines is to present the view of the European Glaucoma Society
(EGS) on the diagnosis and management of glaucoma. Our Guidelines are intended
to support ophthalmologists in managing patients affected by, or suspected of having,
glaucoma. The Guidelines should be considered as recommendations rather than as strict
treatment protocols.
In the last edition, a simplified grading system for rating the strength of recommendation
and the quality of evidence was introduced and has been retained in the present edition.
The strength of recommendation is graded as either I (strong) or II (weak). A strong
recommendation (I) is to be interpreted as “we recommend” and/or “very relevant in
clinical practice” and a weak recommendation (II) as “we suggest” and/or “less relevant
in clinical practice”.
The quality of evidence is classified as high (A), moderate (B), low (C) or very low (D). As
an example, high quality evidence would be supported by high quality randomised clinical
trials (RCTs). Observational studies would be typically graded as low-quality evidence.
Consensus from our Panel would be graded as (D).
Clinical care must be individualised to the patient, the treating ophthalmologist

and the socioeconomic milieu. The availability of Randomized Controlled Trials
(RCTs) makes it possible to apply scientific evidence to clinical recommendations.
Irrespective of the relative wealth of each European region, economical factors
must be considered by physicians, in order to provide sustainable healthcare.
The EGS and all contributors disclaim responsibility and all liability for any adverse
medical or legal effects resulting directly or indirectly from the use of any of the
definitions, diagnostic techniques or treatments described in the Guidelines. The EGS
does not endorse any product, procedure, company or organisation.
I.1 Terminology, Classification and Definitions
Classification and disease definitions are arbitrary, and a consensus can be reached
only if they are acceptable to most ophthalmologists on both theoretical and practical
grounds. There are conditions where a precise classification is particularly challenging,
such as in congenital forms associated with other anomalies.
The following factors are to be considered in order to identify and separate the different
glaucoma categories.
1. Anatomy / Structure (See Ch. 1)

Open-angle, closed-angle, optic nerve head, etc.
e.g. clinical signs, exfoliation, pigment dispersion
2. Function (See Ch. 1)
e.g. visual field
3. Intraocular pressure (IOP) level (See Ch. 1)
3.1. At which diagnosis is made (See Ch. 2)
3.2. At which damage occurred (See Ch. 1)
3.3. Target IOP (See Ch. 3.2)12
3.4. General conditions: life expectancy, comorbidities
11
Introduction Chapter
MISSION STATEMENT
The goal of glaucoma treatment is to maintain the patient’s visual function and related quality
of life, at a sustainable cost. The cost of treatment in terms of inconvenience and side effects
as well as financial implications for the individual and society requires careful evaluation (See
Ch. 3). Quality of life is closely linked with visual function and, overall, patients with early to
moderate glaucoma damage have good visual function and modest reduction in quality of life,
while quality of life is considerably reduced if both eyes have advanced visual function loss.
I.2 Treatment Principles
A. Treatment Goals (See Ch. 3.1)

A.1. Quality of life
A.2. Quality of vision
A.3. Cost containment
B. Suggested ways of reaching the goal (see Ch. 3 and 4)

B.1. Selection of patients to be treated
B.1.1. Identification of patients with disease
B.1.2. Identification of patients at risk of developing the disease [I,D]
B.1.2.1. Identification of the clinical entity, possibly using a systematic
classification (See Ch. 2)
B.1.2.2. Consideration of mixed mechanisms
B.1.3. Treatment of the above when actual or expected rate of decay risks
interfering with quality of life [I,C]
B.2. Decreasing the risk of ganglion cell loss since it reduces visual function
- Determine the target IOP for the individual [I,D]. In general, when there
is more advanced damage, lower IOPs are needed to prevent further
progression [I,D]
- IOP lowering [I,A]
- Drugs
- Laser
- Surgery
- Verify the target IOP (See Ch.3.2)
- Monitor the Rate of Progression (Field and Disc) [I,D]
- Adjust management according to ROP
- Blood flow (see Ch. 1 and Ch. 3) or neuroprotection (See Ch. 3.); both
under debate [II,D]
- Consider always compliance, persistence and assiduity of follow-up
B.3. Incorporation of a quality of life measure in the outcome of treatment
C. Audit outcomes e.g. efficacy, safety, cost [I,D] (See Ch. Introduction III)
C.1. Failures include patients suffering from the consequences of insufficient IOP
lowering,
12
Since resources are limited worldwide, the following points are relevant to glaucoma
treatment guidelines:
• prevention of visual disability in those at risk of decreased quality of life;

• avoid widespread treatment of elevated IOP per se;
• enforce effective treatment/follow-up in patients with severe functional loss and/
or rapid progression;
• implement strategies to detect all patients with manifest disease.
These points are supported by the results of Randomized Clinical Trials for glaucoma
(See Chapter Introduction II).
FC I – Suggested Questions for Your

Glaucoma Patient
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© European Glaucoma Society 2014

13
Evaluation of Functional Loss / Time for Individualized Treatment
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Figure 1. Evaluation of functional loss/time for individualised treatment

IOP = the IOP level causing damage
L = the difference of visual function between the age-matched normal and the function at the time of diagnosis
RoP = angle between physiological loss and disease progression, representing progression rate
T = time interval between birth and the time of diagnosis
FACTORS = some of the individual features influencing clinical management (in alphabetical order):
1. Corneal thickness; 2. Family history; 3. Gonioscopy; 4. IOP, mean and fluctuation; 5. Life expectancy;
6. Pigment dispersion/exfoliation; 7. Rate of Progression (RoP); 8. Stage of optic nerve head (ONH)
damage; 9. Stage of VF damage; 10. Systemic diseases
The EGS guidelines are to be adapted to individual patients, socioeconomic

environment, medical facilities, skills of the average ophthalmologist and health
professional, and to available resources
14
II - RANDOMIZED CONTROLLED TRIALS FOR GLAUCOMA

In the following pages we briefly summarize results from the large randomized glaucoma
trials (RCTs, and derive comments relevant to clinical decision-making).
II.1 Treatment Vs No Treatment Trials
II.1.1 Collaborative Normal Tension Glaucoma Study (CNTGS)
CNTGS compared treatment versus no treatment in normal tension glaucoma. Eligible

patients had verified progression or threat to fixation. The primary outcome measure
was disease progression as evident from visual fields or stereo disk photographs.
140 patients were randomized. The treatment goal was a 30% reduction from baseline
IOP, obtained with medications. In patients undergoing surgery a 20% reduction was
accepted.
Summary of results1-5: A 30% reduction from baseline was maintained in nearly 50%
of patients. Progression occurred in 12% (7/61) of treated eyes and 35% (28/79) of
controls.
• A beneficial effect of IOP lowering was found only after the data were censored
for the effect on VF of cataract formation1
• In the intent-to-treat analysis no benefit of treatment was found2
• Cataracts were more common in patients treated with surgery
• No correlation with IOP levels maintained during follow up was found in either
group
• Progression rates varied a lot. The mean progression rate in the untreated arm
was 0.41 dB/year5. Prior documented progression did not increase the risk of
future progression compared to subjects without such history
II.1.2 Early Manifest Glaucoma Trial (EMGT)
EMGT was a randomized, prospective trial comparing treatment versus no treatment

to evaluate the effectiveness of IOP reduction in early, previously untreated open-angle
glaucoma6. Secondary aims were to assess factors related to glaucoma progression, and
to determine the natural history of the disease.
During a population-based screening among 44,243 residents in Sweden, 316 eyes of
255 patients were recruited.
Treated patients received a standardized treatment protocol of laser trabeculoplasty and
topical betaxolol. Treatment or no-treatment remained unchanged as long as definite
progression had not occurred. Primary outcome measure was progression of disease,
defined by sustained increases of visual field loss or optic disc changes6.
Summary of results7-12: This study proves and quantifies the value of IOP reduction in
patients with POAG, NTG and pseudoexfoliation glaucoma.
15
• A 25% decrease of IOP from baseline (mean untreated IOP 20.6 mmHg)
reduced the risk of progression by 50%. Risk of progression decreased 10%
with each mmHg IOP reduction from baseline to the first follow-up visit7
• Risk of progression was smaller with lower baseline IOP values and with a
larger initial IOP drop induced by treatment8
• IOP reduction for the fixed treatment protocol, and for ALT depended very
much on pre-treatment IOP13,14
• Important risk factors for progression were: higher IOP, exfoliation syndrome,
more baseline damage, higher age, disc haemorrhages, thinner CCT (in HTG),
and low blood pressure (in NTG)10
• IOP fluctuation was not a risk factor for progression11
• IOP did not increase but remained constant over time in untreated eyes with
POAG, but increased over time in eyes with exfoliation glaucoma15
• Increase in lens opacity occurred more in the treatment arm than in the control
arm7
• Disease progression rates varied substantially between individual patients.
• Untreated progression rates (natural history) were slower in NTG than in HTG,
while eyes with exfoliation glaucoma progressed much faster16
• Progression criteria were more sensitive than those of AGIS and CIGTS, and
definite progression was associated with a mean worsening of MD of less than
2dB17
• In the great majority of cases progression was found first by perimetry7
• QoL did not differ between treatment arms9
• The frequency of disc haemorrhages was higher with lower IOP and was not
influenced by treatment18
II.1.3 The Ocular Hypertension Treatment Study (OHTS)
The OHTS was a multicentre, randomized, prospective clinical trial, designed to study
the effect of topical ocular hypotensive medication in delaying or preventing the onset
of glaucoma in patients with ocular hypertension (OH)19. 1,636 patients were recruited.
Randomization was between treatment with IOP lowering medications and no
treatment. The treatment goal was to lower the IOP to < 24 mmHg and at least 20%
from baseline. The primary outcome was the development of primary open-angle glaucoma
defined as reproducible visual field defects or reproducible optic disc deterioration. After the
initial results were reported, also the control group received treatment.
Summary of results: Mean IOP reduction was 22.5% in the treated group, but also the
control group showed decrease of IOP, 4.0%
• After 5 years 4.4% of patients in the treated group had developed signs of glaucoma
damage versus 9% in controls (p < 0.0001), a 50% reduction of risk20
• Thus > 90% of untreated patients had not converted to glaucoma after 5 years
• After 13 years 22% of patients who had initially been randomized to the control
group had converted to glaucoma versus 16% in the group that was treated already
at the start of the study21
• POAG conversion was detected first in disc photographs in around 50% of patients
and by field testing in approximately 40%22
16
• Risk factors for progression were: thinner CCT, higher IOP, disc haemorrhages,
older age, larger vertical and horizontal cup-to-disc ratios, greater PSD
• Disc haemorrhages detectable in photographs had been missed at 87% of clinical
examinations and rate of progression was higher in eyes with haemorrhages23
• Cataract formation was more common in the medication group24
• Results obtained from initially untreated patients who were later started on
prostaglandins indicate that monocular trials (at least of prostaglandin drops) may
have very limited value25
• Retinal vein occlusions were uncommon but somewhat more common in the control
group (2.1%) than in the treated group (1.4%), not statistically significant26.
II.1.4 European Glaucoma Prevention Study (EGPS)
The EGPS was a multicentre, randomized, double-masked, placebo-controlled clinical

trial. The aim of this study was to evaluate the efficacy of IOP reduction by dorzolamide
in preventing glaucoma damage in patients with OH. The patients were randomized
into 2 groups: active therapy (dorzolamide) and placebo. Main outcome measures
were visual field and/or optic disc changes27.
Summary of results28: 1,081 patients were enrolled. The median duration of follow-up
was 55 months. The IOP difference between the treatment and the control group was
small. The mean IOP reduction was 15% after 6 months and 22% after 5 years in the
dorzolamide group, but there was also a 9% reduction after 6 months and 19% after 5
years in the placebo group, to a large part attributable to high attrition.
The study failed to detect a statistically significant difference between the chosen
medical therapy and placebo, either in IOP lowering effect, or in the rate of
progression to POAG, and attrition was large28.
The same predictors for the development of POAG were identified independently
in both the OHTS observation group and the EGPS placebo group-baseline older
age, higher intraocular pressure, thinner CCT, larger vertical cup-to-disc ratio, and
higher Humphrey VF pattern standard deviation29.
In a later paper diuretics were pointed as a possible risk factor 30.
17
II.2 Studies Comparing Treatments
II.2.1 Collaborative Initial Glaucoma Treatment Study (CIGTS)
The aim was to find out if glaucoma is better treated by initial treatment with
medications or by immediate filtration surgery 31.
607 patients with newly diagnosed open-angle glaucoma randomized to initial
treatment with either medication or trabeculectomy (with or without 5-fluorouracil).
A target IOP algorithm was used specific for each individual eye. Primary outcome
variables were VF progression and Quality of Life (QoL). Secondary outcome
variables were Visual Acuity (VA), IOP, and cataract formation. No event analysis has
been provided identifying numbers of progressing eyes.
Summary of results32-34: IOP reduction was larger with surgery (48%; mean post
treatment IOP 14-15 mmHg;) than with medications (35%; mean post treatment IOP
17-18 mmHg)35.
• For many years mean perimetric progression (analysed as mean MD among all
subjects) was small in both groups32, but after 8 years 21% of surgical patients and
25% of medical patient had progressed, defined as a worsening of MD by 3 dBs35.
• After adjustment for baseline risk factors, larger IOP variation measures were
associated with significantly worse MD values after 3 to 9 years in the medicine
but not in the surgical group36.
• QoL was initially better in the medically treated group37.
• 1.1% of surgical patients had developed endophthalmitis after 5 years38.
• Patients randomized to the surgery arm underwent cataract surgery more than
twice as often as patients in the medical treatment group33.
• Reversal of optic disc cupping was seen in 13% in the surgical group, but was not
associated with improved visual function39.
• Risk factors for progression have not been reported in a ways similar to that of the
other large RCTs, but risk factors for higher IOP have been, and included higher
baseline IOP, worse field status and lower level of education34.
Inclusion criteria may have allowed recruitment of patients with ocular hypertension resulting
in a case mix with a smaller risk of showing progression.
II.2.2 Advanced Glaucoma Intervention Study (AGIS)
AGIS was a multicentre, prospective randomized study in patients with advanced open-
angle glaucoma patients who could not be controlled by maximum tolerated medical
therapy alone. 591 patients (789 eyes) were randomised between two rather complicated
treatments regimes:
1. ATT: argon laser trabeculoplasty then if needed followed by trabeculectomy and then
by a 2nd trabeculectomy, or
2. TAT: trabeculectomy then argon laser trabeculoplasty if needed, and then
trabeculectomy.
18
Enrolled eyes had consistent elevation of intraocular pressure (IOP) of ≥ 18 mmHg. Patients
with MD worse than 16 dB were excluded thus excluding eyes with really advanced glaucoma
as in several of the other RCTs40.
Summary of results:
• In a post-hoc analysis of patients with 6-years of follow-up or more a eyes with
average IOP > 17.5 mmHg over the first three 6-months visits showed a significantly
more/more frequent visual field deterioration compared to eyes with IOP less than
14 mmHg during the same time. There was no average visual field progression, as
measured by MD, in eyes with IOP < 18 mmHg at 100% of the visits, whereas eyes
with less perfect IOP control showed a mean significant visual field worsening41
• After 7 years mean reduction of IOP was greater for eyes assigned to the TAT protocol,
and the cumulative probability of failure of the first intervention was greater for eyes
assigned to ATT
• The percentage of eyes with decreased visual acuity or visual field progression was
lower for the ATT sequence than for TAT In Afro-American patients, but in Caucasians
results were more favourable in the ATT during the first 4 years, but then switched in
favour of TAT42,43
• The probability of cataract formation after 5 years was high after trabeculectomy,
78 %35. Initial trabeculectomy retarded the progression of glaucoma more effectively
in Caucasians than in Afro-Americans44
• Risk factors associated with progression were older age, longer follow-up, and, not
surprisingly, increasing number of glaucoma interventions45
• A flawed analysis erroneously indicated that IOP fluctuations were a risk factor for
progression45, while a later corrected indicated that such fluctuations were a risk in
NTG only46
• Both ALT and trabeculectomy failed more often in younger patients and in eyes with
higher pre-treatment IOP AGIS investigators47
II.3 Summary
These large RCTs have had enormous importance for glaucoma management. EMGT and
OHTS are the first studies that without doubt showed that IOP reduction reduces rate of
progression in manifest glaucoma and the incidence of glaucoma in ocular hypertension.
In addition the RCTs show that IOP reduction reduces progression also in glaucoma eyes
with normal IOP levels, and that risk reduction with IOP lowering is large; several of the
studies show risk reductions of approximately 10% for every mmHg lower pressure.
Together they also identify the important factors for progression, in glaucoma, e.g., older age,
higher IOP, more damage, pseudoexfoliation and disc haemorrhages, in ocular hypertension
higher IOP, older age, thinner CCT and disc haemorrhages.
The RCTs have demonstrated the value of glaucoma treatment, resulted in more ambitious
treatment and provided a much more solid foundation for evidence-based glaucoma care.
19
III - COST-EFFECTIVENESS OF GLAUCOMA CARE
III.1 Case Detection And Screening for Glaucoma
There are no systematic reviews or studies that provide evidence for direct or
indirect links between glaucoma screening and visual field loss, visual impairment,
optic nerve damage, intraocular pressure, or patient-reported outcomes. Also
economic simulation models of cost effectiveness of screening report inconclusive
results with large uncertainties 48-52.There is no evidence that interventions (e.g.,
training) improve opportunistic case finding 52-54.
III.2 Clinical and Cost Effectiveness of Diagnostic Tests Used for Screening,
Detection and Monitoring for Glaucoma
No randomized screening, diagnostic and follow-up trials reporting the clinical

effectiveness or cost-effectiveness have been published 48, 50, 51, 55. Although there
are numerous comparative diagnostic studies there is no evidence which test or
combination of tests improve patient outcomes at a sustainable cost. There is a high
degree of variability in the design and conduct of largely cross-sectional studies of
diagnostic accuracy of technologies for glaucoma. Diagnostic studies typically compare
the performance of a small number of technologies, and indirect comparisons with other
tests have to be interpreted with caution (e.g., because of differences in population,
study definitions, reference standard, etc.). The risk of bias of diagnostic study designs
is an additional concern48, 50, 51, 55. One of the major challenges to evaluate a diagnostic
test in glaucoma is the lack of a perfect reference standard. There are multiple
diagnostic technologies that can be potentially used to detect glaucoma. Diagnostic
studies have been conducted in a variety of settings (e.g., screening, case detection in
the community, and diagnosis at hospital eye services).
III.3 Treatment of Glaucoma and Ocular Hypertension in Preventing Visual

Disability
There is high-level evidence that treatment (including medical, laser, and surgical
treatments) decrease intraocular pressure and reduce the risk of development (e.g.,
in patients with OHT) and deterioration (i.e., in patients with established glaucoma) of
optic nerve damage and visual field loss compared to no treatment. However, the direct
effects of treatments on visual impairment and the comparative efficacy of different
treatments are not clear. Which treatments improve patient-reported outcomes is also
unclear56. Based on the economic simulation models in the US, UK, Holland, and China,
treating glaucoma appears to be cost effective compared to ‘no treatment’. There is
uncertainty whether to treat none, some or all patients with ocular hypertension48, 57-59.
When treated, the cost-effectiveness models of different therapeutic interventions give
variable results48.
20
Comment:
All published simulation models are based on characteristics of participants enrolled
in relatively small and tight randomized controlled trials (RCTs) which may not include
all important predictors in the general population and every-day practice. In addition,
RCTs may give an optimistic impression of outcomes compared to ‘real life’ with poorer
compliance and adherence to care both in patients and clinicians in implementing the
guide lines and care protocols. As the data of glaucoma induced visual disability are
limited, the blindness rates in the modeling studies have different estimates48. Similarly,
the data on utility values and influence of glaucoma severity in health status are limited.
Retrospective observational data is incomplete and selective. Reliable and ‘realistic’ data
(preferably from large randomized trials or prospective cohorts of ‘usual patients’) is not
available so far48.
III.4 Follow-Up Protocols And Models Of Care
There is no solid evidence of the optimum monitoring schemes, (e.g. frequency and
timing of visits, technologies to be used for detecting progression) for patients with
manifest glaucoma and ocular hypertension. Some modeling and retrospective studies
suggest that more treatment may allow less frequent monitoring visits in ocular
hypertension and stable glaucoma57, 59-61. One RCT suggests that shared care may save
costs62.
21
References
1. Group CN-TGS. Comparison of glaucomatous progression between untreated patients with

normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am
J Ophthalmol 1998;126(4):487-97.
2. Group CN-TGS. The effectiveness of intraocular pressure reduction in the treatment of normal-
tension glaucoma. . Am J Ophthalmol 1998;126(4):498-505.
3. Drance S, Anderson DR, Schulzer M. Risk factors for progression of visual field abnormalities in
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6. Leske MC, Heijl A, Hyman L, Bengtsson B. Early Manifest Glaucoma Trial: design and baseline
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7. Heijl A, Leske MC, Bengtsson B, et al. Reduction of intraocular pressure and glaucoma
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8. Leske MC, Heijl A, Hussein M, et al. Factors for glaucoma progression and the effect of
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9. Hyman LG, Komaroff E, Heijl A, et al. Treatment and vision-related quality of life in the early
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11. Bengtsson B, Leske MC, Hyman L, Heijl A. Fluctuation of intraocular pressure and glaucoma
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12. Heijl A, Leske MC, Bengtsson B, Hussein M. Measuring visual field progression in the Early
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13. Heijl A, Leske MC, Hyman L, et al. Intraocular pressure reduction with a fixed treatment
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14. Heijl A, Peters D, Leske MC, Bengtsson B. Effects of argon laser trabeculoplasty in the Early
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15. Hyman L, Heijl A, Leske MC, et al. Natural history of intraocular pressure in the early manifest
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16. Heijl A, Bengtsson B, Hyman L, Leske MC. Natural history of open-angle glaucoma.
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18. Bengtsson B, Leske MC, Yang Z, Heijl A. Disc hemorrhages and treatment in the early manifest
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19. Gordon MO, Kass MA. The Ocular Hypertension Treatment Study: design and baseline
description of the participants. Arch Ophthalmol 1999;117(5):573-83.
20. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a
randomized trial determines that topical ocular hypotensive medication delays or prevents the
onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120(6):701-13; discussion 829-30.
21. Kass MA, Gordon MO, Gao F, et al. Delaying treatment of ocular hypertension: the ocular
hypertension treatment study. Arch Ophthalmol 2010;128(3):276-87.
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22. Keltner JL, Johnson CA, Anderson DR, et al. The association between glaucomatous visual
fields and optic nerve head features in the Ocular Hypertension Treatment Study. Ophthalmology
2006;113(9):1603-12.
23. Budenz DL, Anderson DR, Feuer WJ, et al. Detection and prognostic significance of optic
disc hemorrhages during the Ocular Hypertension Treatment Study. Ophthalmology
2006;113(12):2137-43.
24. Herman DC, Gordon MO, Beiser JA, et al. Topical ocular hypotensive medication and lens
opacification: evidence from the ocular hypertension treatment study. Am J Ophthalmol
2006;142(5):800-10.
25. Bhorade AM, Wilson BS, Gordon MO, et al. The utility of the monocular trial: data from the
ocular hypertension treatment study. Ophthalmology 2010;117(11):2047-54.
26. Barnett EM, Fantin A, Wilson BS, et al. The incidence of retinal vein occlusion in the ocular
hypertension treatment study. Ophthalmology 2010;117(3):484-8.
27. Miglior S, Zeyen T, Pfeiffer N, et al. The European glaucoma prevention study design and
baseline description of the participants. Ophthalmology 2002;109(9):1612-21.
28. Miglior S, Zeyen T, Pfeiffer N, et al. Results of the European Glaucoma Prevention Study.
Ophthalmology 2005;112(3):366-75.
29. Miglior S, Pfeiffer N, Torri V, et al. Predictive factors for open-angle glaucoma among patients
with ocular hypertension in the European Glaucoma Prevention Study. Ophthalmology
2007;114(1):3-9.
30. Miglior S, Torri V, Zeyen T, et al. Intercurrent factors associated with the development of
open-angle glaucoma in the European glaucoma prevention study. Am J Ophthalmol
2007;144(2):266-75.
31. Musch DC, Lichter PR, Guire KE, Standardi CL. The Collaborative Initial Glaucoma Treatment
Study: study design, methods, and baseline characteristics of enrolled patients. Ophthalmology
1999;106(4):653-62.
32. Lichter PR, Musch DC, Gillespie BW, et al. Interim clinical outcomes in the Collaborative Initial
Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery.
Ophthalmology 2001;108(11):1943-53.
33. Musch DC, Gillespie BW, Niziol LM, et al. Cataract extraction in the collaborative initial glaucoma
treatment study: incidence, risk factors, and the effect of cataract progression and extraction on
clinical and quality-of-life outcomes. Arch Ophthalmol 2006;124(12):1694-700.
34. Musch DC, Gillespie BW, Niziol LM, et al. Factors associated with intraocular pressure
before and during 9 years of treatment in the Collaborative Initial Glaucoma Treatment Study.
Ophthalmology 2008;115(6):927-33.
35. Musch DC, Gillespie BW, Lichter PR, et al. Visual field progression in the Collaborative Initial
Glaucoma Treatment Study the impact of treatment and other baseline factors. Ophthalmology
2009;116(2):200-7.
36. Musch DC, Gillespie BW, Niziol LM, et al. Intraocular pressure control and long-term
visual field loss in the Collaborative Initial Glaucoma Treatment Study. Ophthalmology
2011;118(9):1766-73.
37. Janz NK, Wren PA, Lichter PR, et al. The Collaborative Initial Glaucoma Treatment Study: interim
quality of life findings after initial medical or surgical treatment of glaucoma. Ophthalmology
2001;108(11):1954-65.
38. Zahid S, Musch DC, Niziol LM, Lichter PR. Risk of endophthalmitis and other long-term
complications of trabeculectomy in the Collaborative Initial Glaucoma Treatment Study (CIGTS).
Am J Ophthalmol 2013;155(4):674-80, 80 e1.
23
39. Parrish RK, 2nd, Feuer WJ, Schiffman JC, et al. Five-year follow-up optic disc findings of the
Collaborative Initial Glaucoma Treatment Study. Am J Ophthalmol 2009;147(4):717-24 e1.
40. Brown RH, Lynch M, Leef D, et al. The Advanced Glaucoma Intervention Study (Agis) .1. Study
Design and Methods and Base-Line Characteristics of Study Patients. Controlled Clinical Trials
1994;15(4):299-325.
41. Investigators TA. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship
between control of intraocular pressure and visual field deterioration. Am J Ophthalmol
2000;130(4):429-40.
42. Ederer F, Gaasterland DA, Dally LG, et al. The Advanced Glaucoma Intervention Study
(AGIS): 13. Comparison of treatment outcomes within race: 10-year results. Ophthalmology
2004;111(4):651-64.
43. Investigators TA. The advanced glaucoma intervention study, 6: effect of cataract on visual field
and visual acuity. . Arch Ophthalmol 2000;118(12):1639-52.
44. (AGIS) TAGIS. The Advanced Glaucoma Intervention Study (AGIS): 9. Comparison of
glaucoma outcomes in black and white patients within treatment groups. Am J Ophthalmol
2001;132(3):311-20.
45. Nouri-Mahdavi K, Hoffman D, Coleman AL, et al. Predictive factors for glaucomatous
visual field progression in the Advanced Glaucoma Intervention Study. Ophthalmology
2004;111(9):1627-35.
46. Caprioli J, Coleman AL. Intraocular pressure fluctuation a risk factor for visual field progression
at low intraocular pressures in the advanced glaucoma intervention study. Ophthalmology
2008;115(7):1123-9 e3.
47. (AGIS) TAGIS. The Advanced Glaucoma Intervention Study (AGIS): 11. Risk factors for failure of
trabeculectomy and argon laser trabeculoplasty. Am J Ophthalmol 2002;134(4):481-98.
48. Tuulonen A. Economic considerations of the diagnosis and management for glaucoma in the
developed world. Curr Opin Ophthalmol 2011;22(2):102-9.
49. Vaahtoranta-Lehtonen H, Tuulonen A, Aronen P, et al. Cost effectiveness and cost
utility of an organized screening programme for glaucoma. Acta Ophthalmol Scand
2007;85(5):508-18.
50. Burr JM, Mowatt G, Hernandez R, et al. The clinical effectiveness and cost-effectiveness of
screening for open angle glaucoma: a systematic review and economic evaluation. Health
Technol Assess 2007;11(41):iii-iv, ix-x, 1-190.
51. Ervin AM, Boland MV, Myrowitz EH, et al. Screening for Glaucoma: Comparative Effectiveness.
Rockville (MD)2012.
52. Taylor HR, Crowston, J., Keeffe, J. et al. Tunnel vision: the economic impact of primary open
angle glaucoma – a dynamic economic model. Melbourne: Centre for Eye Research Australia,
2008. www.cera.org.au.
53. Ratnarajan G, Newsom W, French K, et al. The impact of glaucoma referral refinement
criteria on referral to, and first-visit discharge rates from, the hospital eye service: the Health
Innovation & Education Cluster (HIEC) Glaucoma Pathways project. Ophthalmic Physiol Opt
2013;33(2):183-9.
54. Shah S, Murdoch IE. NICE - impact on glaucoma case detection. Ophthalmic Physiol Opt
2011;31(4):339-42.
55. Tarride JE, Burke N, Hopkins RB, et al. New glaucoma diagnostic technologies: a systematic
review of economic studies. Can J Ophthalmol 2011;46(1):89-90.
56. Boland MV, Ervin AM, Friedman DS, et al. Comparative effectiveness of treatments for
open-angle glaucoma: a systematic review for the U.S. Preventive Services Task Force.
24
Ann Intern Med 2013;158(4):271-9.

57. Burr JM, Botello-Pinzon P, Takwoingi Y, et al. Surveillance for ocular hypertension: an evidence
synthesis and economic evaluation. Health Technol Assess 2012;16(29):1-271, iii-iv.
58. Li EY, Tham CC, Chi SC, Lam DS. Cost-effectiveness of treating normal tension glaucoma.
Invest Ophthalmol Vis Sci 2013;54(5):3394-9.
59. van Gestel A. Glaucoma management. Economic evaluations based on a patient level
simulation model. Enschede, Holland: Ipskamp Drukkers, 2012.
60. Hagman J. Comparison of resource utilization in the treatment of open-angle glaucoma between
two cities in Finland: is more better? Acta Ophthalmol 2013;91 Thesis 3:1-47.
61. Crane GJ, Kymes SM, Hiller JE, et al. Accounting for costs, QALYs, and capacity constraints:
using discrete-event simulation to evaluate alternative service delivery and organizational
scenarios for hospital-based glaucoma services. Med Decis Making 2013;33(8):986-97.
62. Holtzer-Goor KM, van Sprundel E, Lemij HG, et al. Cost-effectiveness of monitoring glaucoma
patients in shared care: an economic evaluation alongside a randomized controlled trial. BMC
Health Serv Res 2010;10:312.
25
26
GLOSSARY
5-FU 5-Fluorouracil
AAC Acute Angle-Closure
AC Anterior Chamber
AGIS Advanced Glaucoma Intervention Study
ALPI Argon Laser Peripheral Iridoplasty
ALT Argon Laser Trabeculoplasty
APAC Anterior Chamber Paracentesis
BAC Benzalkalonium Chloride
CACG Chronic Angle-Closure Glaucoma
CAM Complementary And Alternative Medicine
CCT Central Corneal Thickness
CDR Cup/Disc Ratio
CH Corneal Hysteresis
CIGTS Initial Glaucoma Treatment Study
CNS Central Nervous System
CNTGS Collaborative Normal Tension Glaucoma Study
COPD Chronic obstructive Pulmonary Disease
CRF Corneal Resistance Factor
DCT Dynamic contour tonometry
DD Diffuse Defect
ECC Enhanced Corneal Compensation
EGPS European Glaucoma Prevention Study
EGS European Glaucoma Society
EMEA The European Medicines Agency
EMGT Early Manifest Glaucoma Trial
FC Flow Chart
FD Fourier-domain
FDA Food and Drug Administration
FDT Frequency Doubling Technology
FL Fixation Losses
FN False Negatives
FP False Positive
GAPS Glaucoma Adherence and Persistency Study
GAT Goldmann Applanation Tonometry
GHT The Glaucoma Hemifield Test
GON Glaucomatous Optic Neuropathy
GPA Glaucoma Progression Analyses
GPS Glaucoma Probability Score
GSL Goniosynechialysis
GSS Glaucoma Staging System
HEP Heidelberg Edge Perimetry
HIV Human Immunodeficiency Virus
HPG High Pressure Glaucoma
HRP High-pass Resolution Perimetry
HRT Heidelberg Retina Tomography
27
HSV Herpes Simplex Virus

IAC Intermittent Angle-Closure
ICE Irido-Corneal Endothelial syndrome
IDDM Insulin Dependent Diabetes Mellitus
IOL Intraocular Lens
IOP Intraocular Pressure
ISNT Inferior-Superior-Nasal-Temporal rule
ITC Iridotrabecular Contact
LPI Laser Peripheral Iridotomy
LR Likelihood Ratio
LD Localized Defect
LTP Laser Trabeculoplasty
LV Loss Variance
MAO Monoamine Oxidase
MD Mean Defect
MMC Mitomycin C
MRA Moorfields Regression Analysis
NCT Non-Contact Tonometry
NF-1 Neurofibromatosis type 1
NF-2 Neurofibromatosis type 2
NFI Nerve Fibre Indicator
NMDA N-Methyl-D-Aspartate
NPG Normal Pressure Glaucoma
OAG Open Angle Glaucoma
OCT Optical Coherence Tomography
OH Ocular Hypertension
OHTS The Ocular Hypertension Treatment Study
ON Optic Nerve
ONH Optic Nerve Head
OPA Ocular Pulse Amplitude
ORA Ocular Response Analyser
OSD Ocular Surface Disease
PAC Primary Angle-Closure
PACG Primary Angle-Closure Glaucoma
PACS Primary Angle-Closure Suspect
PAS Peripheral Anterior Synechiae
PCG Primary Congenital Glaucoma
PC-IOL Anteriorly Dislocated Posterior Chamber Intraocular Lens
PCL Posterior Chamber Intraocular Lens
PDS Pigment Dispersion Syndrome
PDT Photo Dynamic Therapy
PEX Pseudoexfoliation
PFV Persistent Fetal Vasculature
PG Pigmentary Glaucoma
PG Prostaglandin
PI Peripheral Iridotomy
PIOL Phakic Intraocular Lens
28
POAG Primary Open-Angle Glaucoma

POH Pigmentary Ocular Hypertension
PPT Pressure-Phosphene Tonometer
PSD Pattern Standard Deviation
RCT Randomized Controlled Trial
RNFL Retinal Nerve Fiber Layer
RT Rebound Tonometer
SAP Standard Automated Perimetry
SD Standard Deviation
SITA Swedish Interactive Threshold Algorithm
SLT Selective Laser Trabeculoplasty
SPK Superficial Punctate Keratitis
SWAP Short Wavelength Automated Perimetry
TCA Topographic Change Analysis
TDO Time Domain
TM Trabecular Meshwork
UBM Ultrasound Biomicroscopy
UGH Uveitis-Glaucoma-Hyphema Syndrome
VEGF Vascular Endothelial Growth Factor
VF Visual Filed
VFI Visual Field Index
VZV Varicella Zoster Virus
XFG Exfoliative Glaucoma
XFS Exfoliation Syndrome
YAG Yttrium-Aluminium-Garnet
29
30
CHAPTER 1
Patient
Examination
31
Patient
Examination
1.1 - INTRAOCULAR PRESSURE (IOP) AND TONOMETRY

The intraocular pressure (IOP) in the population is approximately normally distributed
with a right skew. The mean IOP in normal adult populations is estimated at 15-16
mmHg, with a standard deviation of nearly 3.0 mmHg1-10. Traditionally, normal IOP has
been defined as two standard deviations above normality, i.e. 21 mmHg, and any IOP
above this level is considered to be elevated. The level of IOP is a major risk factor
for the development of glaucoma and its progression. For example, the risk of having
glaucoma for those with IOP measurements of 26 mmHg or greater is estimated to be
12 times higher than that for those with IOP within the normal range1.
IOP diurnal variations can be substantial and are larger in glaucoma patients than in
healthy individuals. Evaluating the IOP at different times of the day can be useful in
selected patients [II,D].
1.1.1 Methods of measurement (tonometry)
Tonometry is based on the relationship between the intraocular pressure and the
force necessary to deform the natural shape of the cornea by a given amount (except
Dynamic Contour Tonometry, see below). Corneal biomechanical properties, such as
thickness and elasticity, can affect the IOP measurements (Table 1.1). Tonometers can
be described as contact or non-contact. Some instruments are portable and hand-held
(e.g., Icare, Tonopen).
1.1.1.1 Goldmann applanation tonometry (GAT)
The most frequently used instrument, and the current reference standard [I,D], is the
Goldmann applanation tonometer (GAT), mounted at the slit lamp11. The method involves
illumination of the biprism tonometer head with a blue light (obtained using a cobalt filter)
that is used to flatten the anesthetised cornea which has fluorescein in the tear film. The
scaled knob on the side of the instrument is then turned until the inner border of the two
hemi-circles of fluorescent tear meniscus, visualized through each prism, just touch (Fig. 1.1).
There are potential problems of using GAT in that contact with the tear film and the cornea
may raise concerns regarding transmissible disease. Chemical disinfection and disposable
tonometer heads are used with the hope to reduce the risk of cross infection [I,D].
Errors with GAT can be due to incorrect technique (Fig. 1.2) and to the biological
variability of the eye and orbit. Of particular note is the influence of the central corneal
thickness (CCT). A tight collar or tie, Valsalva’s manoeuvre, breath-holding, squeezing
the lids or the examiner touching the lids can all falsely increase the IOP reading.
33
Patient Examination
1.1.1.2 Alternative tonometers (in alphabetical order):
Table 1.2 below summarises the comparisons of IOP between other tonometers and
GAT. A substantial proportion of IOP results differ by more than 2 mmHg12. A complete
list of all available technologies is beyond the scope of the guidelines.
% Dynamic contour tonometry (DCT, or Pascal)

This slit-lamp mounted instrument contains a sensor tip with concave surface contour
and a miniaturized pressure sensor. The result and a quality score measure are
provided digitally. This technique is reportedly less influenced by corneal thickness
than GAT. The DCT additionally measures the ocular pulse amplitude (OPA) which is
the difference between the mean systolic and the mean diastolic IOP13-18.
% Non-contact tonometry (NCT)

The NCT or air puff tonometry uses a rapid air pulse to flatten the cornea, thus
working on the same basic principle as the Goldmann tonometer. The advantages
include speed, no need for topical anaesthesia and no direct contact with the eye.
There are several models available in the market. Some patients have found the
air puff uncomfortable. There is currently insufficient evidence to replace GAT with
non-contact tonometry19, 20.
% Ocular Response Analyser (ORA)

The ORA utilises air-puff technology to record two applanation measurements, one
while the cornea is moving inward, and the other as the cornea returns. The average
of these two IOP values provides a Goldmann-correlated IOP measurement (IOPG).
The difference between these two IOP readings is called Corneal Hysteresis (CH),
a result of viscous damping in the corneal tissue. The CH measurement provides a
basis for two additional new parameters: Corneal-Compensated Intraocular Pressure
(IOPCC) and Corneal Resistance Factor (CRF). The IOPCC is a measurement that is
less affected by the corneal properties. Four good quality readings per eye are
recommended21-25 [II,D].
% Ocuton S
The Ocuton S is a self-measurement applanation tonometer that calculates and
displays the IOP value automatically through direct contact of the measuring prism
with the cornea. Topical anaesthetic is required26, 27.
% Pneumatonometry
The pneumatonometer relies on the Mackay-Marg principle and measures
intraocular pressure noninvasively through applanation tonometry28.
The sensing unit of the pneumatonometer, covered with a Silastic diaphragm,
pressurized air flows constantly through an opening centrally into the space
between the nozzle and the diaphragm. When in contact with the cornea, the
pressure of the airstream is increased and this increment is converted into IOP. This
raises the pressure of the air stream in the central chamber, and this increment
is converted into IOP29. Measured values are usually higher than with GAT30, this
technique can be useful for non cooperating, bedridden patients or infants.
34
Patient Examination
% Rebound tonometry (Icare)

The rebound tonometer is a simple portable device. Although it is a contact
tonometer topical anaesthetic drops are not required and the tonometer has a
disposable tip to minimise the risk of cross-infection. The device processes the
rebound movement of a rod probe resulting from its interaction with the eye;
rebound increases (shorter duration of impact) as the IOP increases.
Six measurements are taken to provide accurate measurement results. The
rebound tonometer can be particularly useful in children [II,C]. The Icare ONE Home
device is a variation that has been designed for self tonometry31-35.
% Tono-Pen
The Tono-Pen is a hand-held portable tonometer that determines IOP by making
contact with the cornea (central contact is recommended) through a probe tip,
causing applanation/indentation of a small area. Topical anaesthetic eye drops are
used. After four valid readings are obtained the averaged measurement is given
together with the standard error36-38.
Both the Icare and Tono-Pen are useful for patients with corneal disease and surface
irregularity as the area of contact is small [II,C].
% Transpalpebral tonometry
This type of tonometry includes devices that measure IOP through the eyelid
avoiding direct corneal contact. The Diaton® tonometer is a hand held, pen like,
portable device applying this principle. The pressure-phosphene tonometer (PPT)
(Proview®) has been developed as a self measurement tonometer. The threshold
pressure for creating a phosphene (perception of light) associated with the localised
indentation is the estimated IOP. There is insufficient evidence to replace GAT by
transpalpebral tonometry39-43 [I,D].
% Triggerfish® (Sensimed) has a sensor embedded in a contact lens, based on strain

gauges claimed to record changes in the area of the corneo-scleral junction. There is
no evidence to support the use of this device in clinical practice44.
1.1.2 Intraocular pressure and central corneal thickness
Central corneal thickness (CCT) influences GAT readings (Table 1.1). However, there is
no agreement as to whether there is a validated and useful correction algorithm for GAT
and CCT. The normal distribution of CCT is 540 ±30 μm (mean +/- SD)45.
CCT variations after corneal refractive surgery make difficult to interpret GAT46. A record
of pre-operative CCT is helpful to manage patients undergoing refractive surgery [II,D].
Except for unusual circumstances, there is no evidence to support the use

of methods alternative to Goldmann applanation tonometry for the routine
management of patients suspected of having, or that do have, glaucoma.
35
Patient Examination
Technique of Goldmann Applanation Tonometry.
Figure 1.1. When there is contact between the tonometer prism (left) and the cornea, the stained tear
meniscus can be observed through the prism.
36
Patient Examination
Correct Alignement of
Fluorescein Ring
A Regular cornea Astigmatic cornea
Reading on dial Higher than IOP Lower than IOP
Centration correct correct incorrect

Fluorescein ring too thick too thin correct
Reading on dial falsely low falsely high unreliable
Figure 1.2. Correct technique (A): the prism is correctly aligned to the centre of the cornea and the
applied pressure is then adjusted until the inner part of the semicircles touch each other. When the
reading is taken before the semicircles are aligned as in (A), the applanation pressure will not cor-
respond correctly to the IOP shown on the dial (B). Incorrect alignment can combine with incorrect
amount of fluorescein, adding error on error (C).
Note: In case of high or irregular astigmatism, corrections should be made. One

option is to do two measurements, the first with the biprism in horizontal position and
the second in vertical position and the readings should be averaged. Another way of
correcting large regular astigmatism (> 3 D) is to align the red mark of the prism with
the axis of the minus cylinder.
37
Patient Examination
Table 1.1 Influence of corneal status, thickness and tear film on the intraocular pressure
(IOP) value measured with the Goldmann Applanation Tonometry.
Cornea Status IOP reading erroneously high IOP reading erroneously low
Thin central cornea x
Thick central cornea x
Epithelial oedema x
Excessive tear film x
Insufficient tear film x
Corneal refractive surgery* x
* Corneal refractive surgeries alter tonometry reading since they modify thickness, curvature and
structure of the cornea.
Table 1.2 Differences in IOP between different tonometers and Goldmann Applanation
Tonometry (GAT). Pooled estimates and summary 95% limits of agreement11-45.
Mean
Difference
95% Confidence 95% Limits of
Tonometer between % within 2 mmHg
Interval Agreement
Tonometer and
GAT
DCT 1.8 +1.3 +2.3 -3.0 +6.6 47
NCT 0.3 -0.1 +0.7 -3.5 +4.0 69
ORA 1.5 +0.9 +2.2 -4.3 +7.3 45
Ocuton S 2.7 -1.2 +6.7 -4.0 +9.6 33
RT-(Icare) 0.9 +0.5 +1.5 -4.3 +6.3 51
TonoPen 0.2 -0.4 +0.9 -5.2 +5.7 52
Transpalpebral -0.5 -1.3 +0.3 -7.0 +5.9 45
DCT = Dynamic Contour Tonometer; NCT = Non-Contact Tonometer; ORA = Ocular

Response Analyzer; RT = Rebound Tonometer.
38
Patient Examination
1.2 - GONIOSCOPY
Gonioscopy is an important part of the comprehensive adult eye examination and
essential for evaluating patients suspected of having, or who do have glaucoma47-50 [I,D]
(See FC II).
The purpose of gonioscopy is to inspect the anterior chamber angle. It is based on the
recognition of angle landmarks and must always include an assessment of at least the
following:
a) level of iris insertion, both true and apparent

b) shape of the peripheral iris profile
c) width of the angle approach, i.e.: angular separation between the corneal
endothelium and the anterior surface of the peripheral iris
d) degree of trabecular pigmentation
e) areas of iridotrabecular apposition or synechia
FC II - Diagnostic Gonioscopy in Open Angle

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39
Patient Examination
1.2.1 Anatomy
Reference landmarks
Schwalbe’s line: this collagen condensation of the Descemet’s membrane between the
trabecular meshwork and the corneal endothelium appears as a thin translucent line.
Schwalbe’s line may be prominent and anteriorly displaced (posterior embryotoxon), or there
may be heavy pigmentation over it. A pigmented Schwalbe’s line may be misinterpreted
as the trabecular meshwork, particularly when the iris is convex. Indentation (‘dynamic’)
gonioscopy and the corneal wedge method are helpful to distinguish between the structures
by reliably identifying Schwalbe’s line.
Trabecular Meshwork (TM): this extends posteriorly from Schwalbe’s line to the scleral
spur. Close to Schwalbe’s line is the non-functional trabecular meshwork, blending into
to the posterior, functional and usually pigmented TM. If the TM is not seen in 180° or
more, angle closure is present. Most difficulties concerning examination of the TM relate
to the determination of whether observed features are normal or pathological (particularly
pigmentation), blood vessels and iris processes.
Pigmentation: pigment is found predominantly in the posterior meshwork. It is seen in

adults, rarely before puberty and the extent can be highly variable. The most common
conditions associated with dense pigmentation are: pseudoexfoliation syndrome, pigment
dispersion syndrome, previous trauma, previous laser treatment of the iris, uveitis and after
an acute angle-closure attack.
Blood vessels: these are often found in normal iridocorneal angles. They characteristically
have a radial or circumferential orientation, have few anastomoses and do not run across the
scleral spur. They can be seen most easily in subjects with blue irides. Pathological vessels
are usually thinner, have a disordered orientation and may run across the scleral spur to
form a neovascular membrane. Abnormal vessels are also seen in Fuchs’ heterochromic
iridocyclitis and chronic anterior uveitis.
Schlemm’s canal: is not normally visible, though it may be seen if it contains blood. Blood
reflux from episcleral veins may occur in cases of carotid-cavernous fistulae, Sturge Weber
syndrome, venous compression, ocular hypotony, sickle cell disease or due to suction from
the goniolens.
Scleral spur: is of white appearance and located between the pigmented TM and the ciliary body.
Iris processes: are present in one third of normal eyes, more evident in younger subjects.
When numerous and prominent they may represent a form of Axenfeld-Rieger syndrome/
anomaly. They are distinguished from goniosynechiae which are thicker and wider and may
go beyond the scleral spur.
Ciliary band and iris root: the iris insertion is usually at the anterior face of the ciliary body,
though the site is variable. The ciliary band may be wide, as in myopia, aphakia or following
trauma, or narrow or not seen as in hyperopia and anterior insertion of the iris.
40
Patient Examination
1.2.2 Techniques
Gonioscopy is an essential part of all glaucoma patients evaluation [I,D]. Gonioscopy should
always be performed in a dark room, using the thinnest slit beam, taking care to avoid
shining the light through the pupil because of pupil constriction in light exposure51, 52 [I,D].
There are two main techniques for viewing the anterior chamber angle:
% Direct Gonioscopy
The use of some contact goniolenses like the Koeppe or Barkan lens permits the
light from the anterior chamber to pass through the cornea so that the angle may
be viewed (Fig. 1.3 top).
% Indirect Gonioscopy
The light from the anterior chamber is made to exit via a mirror built into a contact
glass (Fig. 1.3.bottom).
Some features of this technique are:
Patients must lie on their back

• Gives a direct view of the anterior
chamber angle
• Good magnification
• Easy orientation for the observer
• Possible simultaneous comparison of
both eyes
Requires high magnification with
illuminated loupes or portable slit-lamp.
Angle view possible with direct
ophthalmoscope by dialing high plus
lens
Some features of this technique are:
• Patient must be at the slit lamp

• Indirect view of the anterior chamber
angle
• Faster than direct gonioscopy during
routine ophthalmological exam
• It can be used to see the fundus (using
the central part of the lens) at the slit
lamp
• Inability to compare the two eyes
simultaneously
Figure 1.3
41
Patient Examination
The most common Gonioscopy lenses:

Direct Koeppe (contact fluid required)
Layden (sized for infants; contact fluid required)
Worst
Indirect Posner or Zeiss or Sussman 4 mirror (contact fluid not required)
Goldmann lens, 1 to 4 mirrors (contact fluid required)
CGA 1.4© Lasag (contact fluid required)
Magnaview (contact fluid required)
1.2.2.1 ‘Dynamic indentation’ gonioscopy
It is recommended to use a small diameter lens for indentation (e.g.: 4-mirror) [I,D].
When gentle pressure is applied by the lens on the center of the cornea, the aqueous
humour is pushed back. In appositional angle-closure, the angle can be re-opened. If
there is adhesion between the iris and the meshwork, as in goniosynechiae, that portion
of angle remains closed (Fig. 1.4(3)).
When pupillary block is the prevalent mechanism the iris becomes peripherally concave
during indentation. In iris plateau configuration this iris concavity will not be extended by
indentation to the extreme periphery, which is a sign of anteriorly placed ciliary processes
(double hump sign). When the crystalline lens has a particularly prominent role, indentation
causes the iris to move only slightly backwards, retaining a convex profile (Fig. 1.4(4)).
To differentiate appositional from synechial closure “indentation” or “dynamic”

gonioscopy is essential.
42
Patient Examination
1 2
3 4
© European Glaucoma Society
Figure 1.4. Dynamic indentation gonioscopy. When no angle structure is directly visible before inden-
tation, angle-closure may be present, and it can be synechial or appositional (1). If during indenta-
tion the iris moves peripherally backwards and the angle recess widens (2), the picture in (1) is to
be interpreted as appositional closure and a suspicion of relative pupillary block is raised (2). When
during indentation the angle widens but iris strands remain attached to the angle outer wall (3), the
picture in (1) is to be interpreted as synechial closure. A large and/or anteriorly displaced lens causes
the iris to move only slightly and evenly backwards during indentation (4) making the lens a likely
component of angle-closure.
1.2.2.2 Gonioscopy technique without indentation
With indirect Goldmann-type lenses it is preferable to start by viewing the inferior

angle, which often appears wider than the superior angle, because it is easier to
identify the different structures. Then to continue rotating the mirror [II,D]. The anterior
surface of the lens should be kept perpendicular to the observation axis so that the
appearance of the angle structure is not changed as the examination proceeds. The
four quadrants are examined by a combination of slit-lamp movements and prism
rotation.
In case of a narrow approach, it is possible to improve the visualization of the angle
recess by asking the patient to look in the direction of the mirror being used.
43
Patient Examination
Practical points
% Related to the technique
Gonioscopy should be performed in a dark room and with a small slit beam [I,D].
The most widely used technique is indirect gonioscopy where the angle is viewed in
a mirror of the lens. The position of the globe is of importance. Angle width grading
must be performed with the eye in primary position to avoid misclassification. If the
patient looks in the direction of the mirror the angle appears wider and vice versa.
A second pitfall is inadvertent pressure over the cornea, which will push back the
iris, and gives an erroneously wide appearance to the angle. This occurs when the
diameter of the lens is smaller than the corneal diameter e.g.: 4-mirror lenses. With
a large diameter goniolens, indentation is transmitted to the periphery of the cornea
distorting the angle.
% Related to the anatomy
Recognition of angle structures may be impaired by variations in the anterior
segment structures like poor pigmentation, iris convexity or existence of pathological
structures.
Pharmacological mydriasis
Dilation of the pupil with topical or systemic drugs can trigger angle-closure. Angle-closure
attacks can occur, even bilaterally, in patients treated with systemic parasympatholytics
before, during or after abdominal surgery and has been reported with many systemic
drugs such as serotonergic ‘appetite’ suppressants53.
Although pharmacological mydriasis with topical tropicamide and neosynephrine is safe
in the general population even in eyes with a narrow approach, IOP elevation can occur
in occasional patients (approx. 10%)54. Screening with van Herick’s test can detect
angles at risk prior to dilating (Fig. 1.6).
Systemic drugs with effects on the angle

Theoretically, although any psychoactive drugs have the potential to cause angle-
closure, it is unlikely that pre-treatment gonioscopy findings alone are of help to rule
out such risk. In eyes with narrow angles, it makes sense to repeat gonioscopy and
tonometry after initiation of treatment [II,D]. Prophylactic laser iridotomy needs to be
evaluated against the risks of angle-closure or of withdrawal of the systemic treatment
[II,D]. (See Ch. 2.4). None of these drugs is contraindicated per se in open-angle
glaucoma. Ciliochoroidal detachment with bilateral angle-closure has been reported
after oral sulpha drugs and topiramate55.
1.2.3 Grading
The use of a grading system for gonioscopy is highly desirable48, 56, 57 [I,D]. It stimulates the
observer to use a systematic approach in evaluating angle anatomy, it allows comparison
of findings at different times in the same patients, or to classify different patients.
The Spaeth gonioscopy grading system is the most detailed (Fig. 1.5)48.
Other practical grading systems are those of Shaffer58 and Kanski59; both are based on
angle width and visibility of the structures.
44
Patient Examination
Document the insertion level of the iris root before and during compression dynamic
gonioscopy
1 Insertion of iris root

A Anterior to Schwalbe's line
B Behind Schwalbe's line
C On the Scleral Spur
D Behind the Scleral Spur
E On the Cillary Band
2 Angular width of angle recess
Slit
10°
20° 10°
30° narrow
40° 20°
30°
wide
40°
3 Configuration of the peripheral iris

s (steep)
r (regular)
q (queer) s Steep, anteriorly convex
r Regular
q Queer, anteriorly concave
4 Plateau Configuration
Figure 1.5. The Spaeth Grading System of gonioscopy finding.
45
Patient Examination
s
a b a
b
s
Slit
Beam
r
Observe
b/a: Grade:
Figure 1.6. The Van Herick test.
46
Patient Examination
1.2.3.1 Slit lamp-grading of peripheral AC depth - The Van Herick Method
The Van Herick grading is an important part of any comprehensive eye examination
(Fig. 1.6) [II,D]. This method is very useful if a goniolens is not available 57, 60 [I,D]
and can identify the need for gonioscopy in patients not otherwise suspected of
glaucoma but it is not a substitute for gonioscopy. This technique is based on the
use of corneal thickness as a unit measure of the depth of the anterior chamber at
the furthest periphery, preferably on the temporal side.
Grade 0 represents iridocorneal contact.
A space between iris and corneal endothelium of < 1/4 corneal thickness, is a Shaffer
grade I. When the space is ≥ 1/4 < 1/2 corneal thickness the grade is II. A grade III is
considered not occludable, with an irido/endothelia l distance ≥ 1/2 corneal thickness.
1.2.4 Anterior Segment Imaging Techniques
UBM, anterior segment OCT and Scheimpflug cameras can be useful in some
circumstances. Added to gonioscopy, these techniques help elucidate the mechanism
of angle-closure in many cases [II,D]. Due to their limited availability and costs
however, they are applied to cases which are most difficult to interpret 61-69. UBM
is very helpful in diagnosis behind the iris and the pigmented epithelium (tumours,
cysts). Anterior segment OCT and Scheimpflug cameras are suitable for volumetric
measurements and documentation of the dynamics of the chamber angle at different
light conditions. These instruments currently give information only on the examined
sector and not about the total circumference. None of these imaging methods
provides sufficient information about the anterior chamber angle anatomy to be
considered a substitute for gonioscopy70-89
47
Patient Examination
1.3 - OPTIC NERVE HEAD AND RETINAL NERVE FIBRE LAYER

Glaucoma changes the appearance of the optic nerve head (ONH) and the retinal nerve
fibre layer (RNFL) in a characteristic fashion.
Contour changes can best be appreciated with a magnified stereoscopic view. Therefore
the initial examination, and follow-up examinations for contour change, should be
made preferably through a dilated pupil [I,D]. Interim examinations, aimed at detecting
striking features such as disc haemorrhages, may be performed through an undilated
pupil stereoscopic examination of the posterior pole is best performed with a:
• Indirect non-contact fundus lens with sufficient magnification at the slit-lamp or
• Direct contact fundus lens at the slit-lamp
The direct ophthalmoscope is also useful for ONH and RNFL examination. Although three-
dimensional information using parallax movements is possible, binocular examination
through a dilated pupil is superior. The clinical evaluation of the ONH and RNFL should
assess the following features [I,D].
1.3.1 Clinical Examination - Qualitative
1.3.1.1 Neuroretinal Rim
In a healthy eye, the shape of the rim is influenced by size, shape and tilting of the optic
nerve head. The disc is usually slightly vertically oval, often more so in black subjects
who may also have larger discs. In normal sized discs, the neuroretinal rim is typically at
least as wide at the 12 and 6 o’clock positions as elsewhere and usually widest (83%
of eyes) in the infero-temporal sector, followed by the supero-temporal, nasal and then
temporal sectors (the ‘ISNT’ rule, see fig. 1.10)90.
This pattern is less obvious in larger discs, in which the rim is distributed more evenly
and in a smaller discs where cupping may not be evident. Larger and a smaller discs
are harder to interpret: e.g., in small discs the changes associated with glaucoma
may not result in cupping, but ‘saucerization’ of the disc surface instead, and in large
optic discs the normal rim is relatively narrow and can potentially be misinterpreted as
glaucomatous.
The exit of the optic nerve from the eye may be oblique, giving rise to a tilted disc.
Tilted discs are more common in myopic eyes, and show a wider, gently sloping rim in
one disc sector and a narrower, more sharply-defined rim in the opposite sector. Discs
in highly myopic eyes are even harder to interpret.
Glaucoma is characterized by progressive narrowing of the neuroretinal rim. The pattern
of rim loss varies and may take the form of diffuse narrowing, localized notching, or
both in combination (Fig. 1.7). Narrowing of the rim, while occurring in all disc sectors,
is generally more common and greatest at the inferior and superior poles91-95
48
Patient Examination
A1 A2
Normal B1 B2
ONH
C1 C2
D1 D2
Figure 1.7. Progression of glaucomatous damage at the optic disc:

Early localized loss (A1), advancing to localized plus diffuse rim loss (A2).
Early localized rim loss, polar notches (B1); more advanced polar notches (B2).
Diffuse or concentric rim loss, early (C1); advanced (C2).
Diffuse rim loss (D1), followed by localized r i m loss (notch) (D2).
49
Patient Examination
1.3.1.2 Retinal nerve fibre layer
The RNFL appearance is best assessed with a red-free (green) photograph. Clinically, the
RNFL can be assessed with the red-free light or a short, narrow beam of bright white light at
high magnification to explore the parapapillary region. In healthy eyes, smaller retinal vessels
are embedded in the RNFL. The RNFL surface is best seen if the focus is adjusted just
anterior to the retinal vessels.
The fibre bundles are seen as silver striations. About two disc diameters from the disc
the RNFL thins and feathers out. Slit-like, groove-like, or spindle-shaped apparent defects,
narrower than the retinal vessels, may be seen in the normal fundus. The RNFL becomes less
visible with age, and is more difficult to see in less pigmented fundi.
Defects are best seen within two disc diameters of the disc. Focal (wedge and slit) defects
are seen as dark bands, wider than retinal vessels and extending from the disc margin, unless
obscured by vessels. These focal defects are more easily seen than generalized thinning of
the RNFL, which manifests as a loss of brightness and density of striations. When the RNFL
is thinned, the blood vessel walls are sharp and the vessels appear to stand out in relief
against a matt background. The initial abnormality in glaucoma may be either diffuse thinning
or localized defects. Since the prevalence of RNFL defects is < 3% in the normal population,
their presence is likely to be pathological96-98.
1.3.1.3 Optic disc haemorrhages
The prevalence of small (‘splinter’) haemorrhages on or bordering the optic disc has been
estimated to be ≤ 0.2% in the normal population99. On the other hand, a large proportion of
glaucoma patients have optic disc haemorrhages (ODHs) at one time or another (Fig. 1.8). They
are very often overlooked at clinical examinations, and are easier to find in photographs100-103.
Many studies have shown that ODHs are associated with disease progression.
Figure 1.8. Optic disc

haemorrhage.
Splinter
Haemorrhage
of the Disc
50
Patient Examination
1.3.1.4 Vessels at the optic disc
Narrowing of the neuroretinal tissue will change the position of the vessels at the optic
disc with bending, bayoneting or baring of circumlinear vessels. Those positional changes
are particularly important to observe when looking for progression, in comparison to a
baseline photo.
1.3.1.5 Parapapillary atrophy
Parapapillary atrophy can be differentiated into an Alpha zone, which is present in almost
any eye, and into a Beta zone, which is present in approximately 25% of normal eyes and
in a significantly higher percentage of eyes with glaucoma104-106.
The Alpha zone has been defined as irregular hyperpigmentation and hypopigmentation
and it is located in the periphery of parapapillary atrophy. The Beta zone is characterized
by visible sclera and visible large choroidal vessels and a location between the
peripapillary ring and Alpha zone. Both zones are usually located at the temporal margin
of the optic disc, more often in the inferotemporal region than in the superotemporal
region. Histologically, the Alpha zone corresponds to irregularities in the retinal pigment
epithelium, and the Beta zone shows a complete loss of retinal pigment epithelium, an
almost complete loss of photoreceptors and a closure of the choriocapillaris. The Beta
zone may be associated with a greater amount of glaucomatous optic neuropathy and a
higher risk of further progression of glaucoma107. The location of the Beta zone outside
the optic disc spatially correlates with the location of the most marked loss of neuroretinal
rim inside of the optic disc, together with the longest distance to the central retinal vessel
trunk in the optic nerve head104. In clinical routine, a large ophthalmoscopical Beta zone (in
particular in non-myopic eyes) should be regarded as an extra clue, and not as a definite
sign of glaucoma (Fig. 1.9) [I,C].
Beta Zone
Beta Zone Figure 1.9. ONH with
parapapillary atrophy.
The Alpha zone is located
peripheral to beta zone,
and is characterized
by irregular hypo- and
hyperpigmentation.
The Beta zone of atrophy is
adjacent to the optic disc
edge, external to Elschnig’s
ring (a white circular band
that separates the intra- from
the peri-papillary area of
the optic disc), with visible
sclera and large choroidal
vessels.
Alpha
AlphaZone
Zone
51
Patient Examination
1.3.1.6 The ISNT rule
In normal eyes with a normal optic disc shape, with a greater vertical diameter,
the neuroretinal rim shows a characteristic shape: it is usually widest at the inferior
disc pole, followed by the superior disc pole, the nasal disc region, and finally the
temporal disc region108. For mnemonic reasons, this sequence of disc sectors was
abbreviated as “ISNT” (Inferior-Superior-Nasal-Temporal) rule. In many eyes, the rim
can be wider superiorly than inferiorly, however in almost all normal eyes the rim is
smallest in the temporal 60° of the optic nerve head (Fig. 1.10). The most important
letter in the “ISNT”-rule is therefore the “T”. The application of the ISNT rule is
helpful for detecting early glaucomatous optic nerve damage, since in the early
stage of glaucoma, the rim gets smaller preferentially in temporal inferior disc region
or the temporal superior disc region, leading to a rim shape in which the rim can
be equal in width in the inferior or superior region as compared with the temporal
region. For the assessment of the ISNT rule, it is important to consider that the
area of the peripapillary ring does not belong to the neuroretinal rim. It holds true in
particular for the temporal disc region.
7 1
, © European Glaucoma Society

Figure 1.10. The ISNT rule.
52
Patient Examination
1.3.2 Clinical Examination - Quantitative
1.3.2.1 Optic disc size (vertical disc diameter)
The optic disc size greatly varies in the population. The width of the rim and, conversely,
the size of the cup, vary with the overall size of the disc. The mean vertical disc
diameter is approximately 1.5 mm109.
The vertical diameter of the optic disc can be measured at the slit lamp using a
handheld high power convex lens. The slit beam should be coaxial with the observation
axis; a narrow beam is used to measure the vertical disc diameter using the inner margin
of the white Elschnig’s ring as the reference. A correction factor needs to be used
depending on the magnification of the handheld lens (Fig. 1.11).
scale
+60D +78D +90D Superfield

lens
Volk-Nikon Volk Volk-Nikon NC Volk
correction
0.94-1.03 1.13 1.36-1.59 1.50
factor © European Glaucoma Society
Measured vertical diameter of optic disc

Small Medium Large
Disc area <1.6 mm2 1.6 to 2.8 mm2 >2.8 mm2
Volk 60 D <1.65 mm 1.65 to 2.2 mm >2.2 mm
78 D <1.3 mm 1.3 to 1.75 mm >1.75 mm
90 D <1.1 mm 1.1 to 1.45 mm >1.45 mm
Superfield <1.15 mm 1.15 to 1.50 mm >1.5 mm
Digital 1.0x <1.5 mm 1.5 to 1.95 mm >1.95 mm
Super 66 <1.45 mm 1.45 to 1.9 mm >1.9 mm
Nikon 60 D <1.45 mm 1.45 to 1.9 mm >1.9 mm
90 D <0.95 mm 0.95 to 1.25 mm >1.25 mm
Haag-Streit Goldmann <1.3 mm 1.3 to 1.7 mm >1.7 mm
Figure 1.11. Optic disc size assessed at the slit lamp with handheld high power convex lens.
53
Patient Examination
1.3.2.2 Rim Width and Cup/Disc ratio
A large Cup/Disc Ratio (CDR) has been used as a sign of glaucoma damage. However,
the CDR depends on the disc size, and a large CDR in nor ma l large discs may be
erroneously considered glaucomatous and a small CDR in glaucomatous small discs may
be erroneously considered as normal110 (Fig. 1.12). The use of CDR to classify patients
is not recommended and the attention should be focused on the disc rim [I,D].
In healthy eyes, cupping tends to be symmetrical between the two eyes, the vertical
CDR difference being less than 0.2 in over 96% of normal subjects. A difference in
CDR between eyes with equal optic disc size is suggestive of acquired damage and
glaucoma
Small - size
Normal Mid - size Large - size
C/D= 0.3 C/D= 0.5 C/D= 0.8

Figure 1.12. Optic nerve heads with different disc areas but with the same rim area and the same
number of retinal nerve fibres: small size disc (disc area less than 2 mm² and C/D=0.3), mid-size disc
(disc area between 2 and 3 mm², C/D=0.5) and large disc (disc area greater than 3 mm² and C/D=0.8).
54
Patient Examination
1.3.3 Recording of the Optic Nerve Head (ONH) Features
At baseline, some form of imaging is recommended to provide a record of the ONH

appearance [I,D]. If colour photos are not available, a detailed manual drawing is
recommended. Even if it is difficult to draw a good picture of the ONH, the act of making
a drawing encourages a thorough clinical evaluation of ONH [II,D].
Stereoscopic is preferred to non-stereoscopic photography [I,D]. Colour photography
with a 15° field gives optimal magnification. Sequential photographs can be used to
detect progression of optic disc damage.
1.3.3.1 Quantitative Imaging
Quantitative imaging of the optic nerve head, retinal nerve fibre layer and inner macular
layers have been widely used to assist glaucoma diagnosis and to detect glaucomatous
progression during follow-up.
1.3.3.2 Classification
For cross sectional classification, imaging instruments typically provide three potential
outcomes: “within normal limits”, “borderline” and “outside normal limits”. No imaging
device provides a clinical diagnosis but just a statistical result, based on comparison of
the measured parameters with the corresponding normative database of healthy eyes.
Therefore an interpretation of the result in the context of all clinical data is mandatory [I,D].
The clinician should also assess the quality of the image and analysis and judge whether
the normative database is relevant for the particular patient before including the classification
in the assessment of the patient [I,D]. For instance, imaging artefacts and software errors are
quite common and more frequent in eyes that are highly myopic or have very tilted nerves,
and few devices have normative data appropriate to these eyes. The various imaging
technologies have their own advantages and limitations, and their classification shows only
partial agreement in early glaucoma111. In addition, agreement between classification with
quantitative imaging and visual field testing is only moderate in early glaucoma.
1.3.3.3 Detection of progression
Most commercial imaging devices have software for quantifying glaucomatous

progression, including the rate of progression. The classification algorithms described
above should not be used to assess progression [I,D]. In general, normative databases
are not needed for progression analysis because the patient’s baseline images provide
the reference for change. High quality baselines images are, therefore, of considerable
importance. The user should assess the test series for the quality of images and
software analysis before including the software output in the assessment of the patient
[I,D]. Agreement between structural progression and functional deterioration, over the
relatively short duration of reported studies, is only partial or poor112, 113.
Provided the images in a series are of good quality and progression analysis is
55
Patient Examination
consistent over several tests, imaging devices provide useful data, additional to those
gained from visual field testing, concerning a patient’s glaucoma damage.
1.3.3.4 Imaging instruments
A complete list of all available technologies is beyond the scope of the guidelines.
% Heidelberg Retina Tomography (HRT)

The Heidelberg Retina Tomograph (Heidelberg Engineering, Heidelberg, Germany)
is used to profile and measure the three-dimensional anatomy of the optic
nerve head and surrounding tissues. It can also detect progressive changes
in optic nerve head surface topography. To classify an optic nerve head, three
methods can be used: the Moorfields Regression Analysis (MRA), the linear
discriminant analysis formulas and the Glaucoma Probability Score (GPS)114-116.
The classification algorithms tend to over-report ‘outside normal limits’ in large
optic discs. For progression analysis, the software provides a map of surface
height changes compared to baseline (Topographic Change Analysis [TCA]); the
area and volume of changing regions is presented as a plot over time. Graphs
of rim area over time are also available.
% Scanning laser polarimetry (GDx-ECC)

The GDx-ECC instrument (Carl Zeiss Meditech Inc., Dublin, CA, USA) measures
retinal nerve fibre layer thickness around the optic nerve head on the basis of
retardation of the illuminating laser light. All polarizing structures in the eye cause
retardation, especially the cornea. With Enhanced Corneal Compensation (ECC),
polarization artefacts arising both from the anterior segment and behind the
retina are attenuated117. The main parameter to help distinguish healthy subjects
from glaucomatous patients is the NFI (nerve fibre indicator), although clinicians
should also evaluate the distribution of the retinal nerve fibre layer around the
optic disc (the ‘TNSIT’ curve). Trend and change from baseline analyses for
progression are available.
% Optical coherence tomography (OCT)

Optical coherence tomography is based on interferometry. Current instruments,
Fourier-domain (FD) or Spectral domain (SD) and swept-source OCT systems,
provide faster image acquisition, higher resolution and better image segmentation
than time-domain OCT. Several companies produce FD/SD OCT instruments.
Their technical, software and normative database characteristics vary; thus the
values measured with different OCT systems are not interchangeable. Three main
parameter groups are measured and analysed for classification and detection
of progression: Optic Nerve Head, Retinal Nerve Fibre Layer and Ganglion
Cell Complex. In general, the optic nerve head parameters with OCT may be
less informative than the retinal nerve fibre layer and the ganglion cell complex
parameters118. To identify and measure glaucomatous progression with OCT
systems trend analysis of the retinal nerve fibre layer thickness and inner macular
retinal thickness parameters are particularly useful119.
56
Patient Examination
How to use imaging at baseline [II,D]

Glaucoma suspects with normal or unreliable visual field
Glaucoma with early and moderate damage
How to use imaging for monitoring progression [II,D]

Frequency should be similar to that for VF testing
- Patients should be followed with the same test/method to facilitate estimation
of progression [I,D].
- Baseline, repeated within 3 months after baseline, and then up to 4 more
times in the first two years in case of high risk of progression [II,D].
- Baseline, repeated annually, for ocular hypertensives [II,D].
Although knowing the test-retest variability would be indispensable in determining the

optimal frequency of performing imaging tests, in every-day clinical work it seems
currently impossible to take into account the large number of parameters and their
largely variable reproducibility nor to verify the cost effectiveness of imaging for
glaucoma120.
57
Patient Examination
1.4 - PERIMETRY
1.4.1 Perimetry Techniques
Visual field testing is important for the diagnosis of glaucoma, and even more important
for follow-up and management of glaucoma [I,D].
A complete list of all available technologies and strategies is beyond the scope of the
guidelines.
1.4.1.1 Computerised and manual perimetry
Static computerised perimetry should be preferred in glaucoma management. Kinetic e.g.

Goldmann perimetry is not suitable for detection of early glaucomatous field loss and small
defects will often be lost between isopters121.
Computerised perimetry is also less subjective; the results are numerical and tools for
computer-assisted interpretation are available. Manual kinetic perimetry may be helpful in
patients who are unable to perform automated perimetry.
1.4.1.2 Standard Automated Perimetry - SAP
Glaucoma perimetry has become more standardised over time and today the term
Standard Automated perimetry (SAP) is often used. SAP refers to static computerised
threshold perimetry of the central visual field performed with white stimuli on a dimmer
white background.
% Test algorithms and programs
In glaucoma care threshold perimetry is the recommended standard [I,D].
Commonly used threshold algorithms are: ‘SITA Standard’ and ‘SITA Fast’ in
the Humphrey perimeter. SITA Fast has the advantage of reduced test time but
this may come at the cost of increased variability. In the Octopus perimeter the
commonly used threshold algorithms called the ‘Dynamic Strategy’. TOP algorithm
is more rapid, but may have lower resolution than other threshold tests because
threshold values are determined by averaging test results from several adjacent
test point locations122.
Glaucoma perimetry is performed using a Goldmann size III stimulus in the central
25–30° field where the great majority of retinal ganglion cells are located [I,D].
Common test point patterns are the identical 30-2 and 32 test point patterns of
the Humphrey and Octopus perimeters respectively and G1 and G2 patterns of the
Octopus, which cover the central 30°. A commonly used pattern is the 24-2 pattern
of the Humphrey perimeter, which covers a somewhat smaller area and thereby
reduces test time. Only a small amount of information is lost if the smaller patterns
are used as compared to the larger ones, and common test artefacts from, e.g., trial
lens rims or droopy lids are less common with the more central patterns.
% Selecting a test
It is recommended that clinicians select and familiarise themselves with suitable
SAP tests. Patients should be followed with the same test to facilitate estimation of
58
Patient Examination
progression [I,D]. For those with very advanced disease it may be necessary to consider
using a Goldmann size V stimulus rather than size III, or a perimetric strategy which
focuses more closely on the remaining area of visual field. In both perimeters one may
use test point patterns covering only the central 10° of the field in eyes which have only
‘tunnel’ fields left, e.g. the Octopus M1 or M2 or the Humphrey 10-2 [I,D].
The Humphrey Field Analyzer and the Octopus perimeter are the two most commonly
used SAP perimeters in Europe. Other less frequently used SAP perimeters also having
threshold programmes are available.
1.4.1.3 Non-conventional perimetry
Other modalities of computerised perimetry use different stimuli to SAP. Examples are
SWAP (Short Wavelength Automated Perimetry), FDT (Frequency Doubling Technology),
HEP (Heidelberg Edge Perimetry) and HRP (High-pass resolution perimetry or ring
perimetry) and flicker perimetry. There is insufficient evidence that these tests offer any
advantage over SAP123-126.
FC III - Initial Visual Field Evaluation
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59
Patient Examination
1.4.1.4 Patient instructions
The role of the operator is of great importance. To patients who are naive to the test, the
operator must explain what to expect and how to react to stimuli. The operator needs
to be in the vicinity of the perimeter to react to any patient queries [I,D]. A quiet, dimly lit
environment should be ensured. A short demonstration, before the actual test starts, will
also help patients understand the test. The operator should have taken the tests to better
understand the experience of taking the test. It should be explained that most stimuli will
be very dim and even patients with normal visual fields will be expected to ‘miss’ many
stimuli [II,D].
1.4.2 Interpreting test results
1.4.2.1 Printouts
Humphrey and Octopus both provide similar statistical analyses of single field test
results presented on printouts containing maps of the visual field plus visual field
indices and other means of interpreting a test result.
% The numerical threshold map provides the ‘raw’ estimated threshold values a
teach test point location.
% The grey scale or colour coded map provides a graphical representation of the
numerical threshold map.
% The numerical total deviation map shows point-wise differences between the
age-corrected normal threshold value at each test point location and the
measured value.
% The numerical pattern deviation map shows the same values but after correction
for diffuse loss of sensitivity. Thus, it highlights focal loss of sensitivity.
% Probability maps provide the statistical significance of the numerical deviations.
1.4.2.2 Reliability indices
These indices are meant to estimate patient reliability. With proper instructions
almost all patients are able perform reliable tests.
High frequencies of false positive answers (FP), are clearly a sign of poor reliability,
but high frequencies of false negatives (FN) are of relatively little value. High rates
of fixation losses (FL) may indicate poor attention to the fixation target. In most
modern perimeters patients’ fixation is continuously monitored during the test by an
automatic eye/gaze tracker.
The operator has an important role in monitoring in assessing the reliability of the
test as it is performed and informing the clinician e.g. by annotating the test result
if necessary.
60
Patient Examination
1.4.2.3 Visual field indices
Visual field indices are numbers summarising perimetric test results. An useful index
is MD (mean defect in the Octopus system or mean deviation in the Humphrey
system). MD represents the average difference between normal age-corrected
sensitivity values and the measured threshold values at all test point locations. A
new index developed for the Humphrey perimeter is VFI, which is similar to the MD
value but more centrally weighted, expressed in percent rather than in decibels and
more resistant to diffuse loss127, 128.
The global indices include PSD (Humphrey) and LV (Octopus) measure the local
spatial variability of the visual field. PSD and LV can be used for diagnosis, but they
are less informative than the probability maps. Software to produce graphs mapping
visual field loss to expected anatomical regions is available.
1.4.2.4 Recording the visual field indices
A simple method to record serial data from VF is the GSS; this will give a visual
overview, without any statistical support 129, 130
1.4.2.5 Summarising diagnostic features
% The Glaucoma Hemifield Test (GHT)

The Glaucoma Hemifield Test is incorporated in the Humphrey perimeter.
This analysis classifies results as ‘within normal limits’, ‘outside normal
limits’ or ‘borderline’. The classification of outside normal limits is designed
to identify glaucoma. Two more GHT classifications are ‘general depression
of sensitivity’ and ’abnormally high sensitivity which goes hand in hand with
high frequencies of FP responses’.
% The Bebié curve

The Bebié curve or the cumulative defect curve in the Octopus system is
a summary graph of localised and diffuse sensitivity loss. In entirely diffuse
loss the curve of the measured sensitivities is lower than but parallel to the
displayed normal curve. In focal loss the right part of the measured curve
is depressed as compared to the normal reference curve.
% Diagnosis based on clustered points

Clustered test point locations with significantly reduced sensitivity are more
reliable indicators of early glaucomatous field loss than scattered points.
A r ule, which is of te n use d to clas sif y a te st re sult as glaucomatous,
stipulates a minimum of three clustered points with significantly depressed
sensitivity, of which one should have a significance of p<1% [I,D]. Usually,
the test point locations immediately surrounding the blind spot are ignored
in this analysis.
61
Patient Examination
1.4.2.6 Confirmation of classification
Field defects which appear clearly glaucomatous and fit with the clinical picture may
not need confirmation to support a diagnosis [I,D]. Visual fields with subtle defects
may require confirmatory tests. (See FC IV).
The learning effect.

Many subjects show an improvement in performance reflected as improved reliability
and sensitivity over the first few tests.
FC IV - Diagnostic strategy when initial visual field

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62
Patient Examination
1.4.2.7 Assessing progression
In follow-up it is important to know whether the visual field of an eye is deteriorating

and the rate of progression [I,D]. When assessing change from baseline, apparent
progression needs to be confirmed in two or more tests [I,D].
There are two main approaches to computer-assisted progression analyses:
1. Event analyses (designed to answer the question of whether the field has progressed)
With Glaucoma Change Probability Maps (GCPMs) all visual field tests are
compared to baseline consisting of an average of two baseline tests. Test point
locations that have deteriorated more than the expected test-retest variation are
flagged. Eyes that show deterioration of at least three test point locations are
flagged as possibly progressing if the finding is repeated in two consecutive
tests and likely progressing if existing in three consecutive tests. The rules used
in EMGT131 are part of the HVF Analyser’s guided progression analyses (GPA)
program.
2. Trend analyses (quantify the rate of progression)

The perimetric rate of progression is the velocity of worsening of the visual
field, and is usually measured by performing linear regression analysis of the
MD index or the newer VFI index over time. With MD rate of progression is
expressed in dB/year, and with VFI in %/year.
Trend analysis of global indices includes linear regression of MD and VFI for
the Humphrey and linear regression of MD, LV, DD and LD for the Octopus.
The Octopus provides trend analysis of functionally related clusters of test
points. Several stand-alone software programs are available to perform trend
analysis of individual test locations, clusters or global indices, depending on
the product. These include Peridata, PROGRESSOR and Eye Suite. Some of
the systems described above use trend data to try to predict the future status
of the visual field.
1.4.2.8 Number of tests
Commonly used event and trend analyses require at least five and preferably more
tests to detect progression. However in some cases progression may be detected
before this. This demonstrates the need for relatively frequent perimetry in those
eyes where it is considered necessary to find early progression.
Determining the rate of progression of an individual eye requires a long enough
time span (at least two years) and enough field tests. It is important to identify eyes
showing a fast rate of progression at an early stage. Ideally, all newly diagnosed
glaucoma patients should be tested with SAP three times per year during the first
two years after diagnosis [II,D].
63
Patient Examination
1.4.3 Staging of Visual Field Defects
When discussing disease stages in glaucoma, the status of the visual field is often used
as the most important reference. A discrete-levels staging system132, modified from the
Hodapp-Parrish classification133 has been in use for several years.
The GSS use a combination of MD and PSD to chart the stage of damage129, 130.
Staging systems may be of great interest in scientific studies, cost studies et cetera, but
they are of limited value in clinical management.
Ideally for glaucoma management one should be able to detect and quantify disease
progression in small steps rather than identifying only the transition from one stage to
the next [I,D].
The Hodapp Classification
EARLY GLAUCOMATOUS LOSS

a) MD < -6 dB
b) Fewer than 18 points depressed below the 5% probability level and fewer than
10 points below the p < 1% level
c) No point in the central 5 degrees with a sensitivity of less than 15 dB
MODERATE GLAUCOMATOUS LOSS

a) MD < -12 dB
b) Fewer than 37 points depressed below the 5% probability level and fewer than
c) No absolute deficit (0 dB) in the 5 central degrees
d) Only one hemifield with sensitivity of < 15 dB in the 5 central degrees
ADVANCED GLAUCOMATOUS LOSS

a) MD > -12 dB
b) More than 37 points depressed below the 5% probability level or more than
c) Absolute deficit ( 0 dB) in the 5 central degrees
d) Sensitivity < 15 dB in the 5 central degrees in both hemifields
64
Patient Examination
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a screening tool for the assessment of the anterior segment angle. Ophthalmic Surg
Lasers Imaging 2009;40(4):389-98.
87. See JL. Imaging of the anterior segment in glaucoma. Clin Experiment Ophthalmol
2009;37(5):506-13.
88. Liu S, Li H, Dorairaj S, et al. Assessment of scleral spur visibility with anterior segment
optical coherence tomography. J Glaucoma 2010;19(2):132-5.
89. Yip LW, Sothornwit N, Berkowitz J, Mikelberg FS. A comparison of interocular differences
in patients with pigment dispersion syndrome. J Glaucoma 2009;18(1):1-5.
90. Jonas JB, Gusek GC, Naumann GO. Optic disc morphometry in chronic primary open-
angle glaucoma. I. Morphometric intrapapillary characteristics. Graefes Arch Clin Exp
Ophthalmol 1988;226(6):522-30.
91. Tuulonen A, Airaksinen PJ. Initial glaucomatous optic disk and retinal nerve fiber layer
abnormalities and their progression. Am J Ophthalmol 1991;111(4):485-90.
92. Pederson JE, Anderson DR. The mode of progressive disc cupping in ocular
hypertension and glaucoma. Arch Ophthalmol 1980;98(3):490-5.
93. Zeyen TG, Caprioli J. Progression of disc and field damage in early glaucoma. Arch
Ophthalmol 1993;111(1):62-5.
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94. Spaeth GL. Development of glaucomatous changes of the optic nerve. In: (eds) PK, ed.
Varma, R, Spaeth, GL: The optic nerve in glaucoma. Philadelphia: J.B. Lippincott, 1993.
95. Airaksinen PJ, Tuulonen A, Alanko HI. Rate and pattern of neuroretinal rim area
decrease in ocular hypertension and glaucoma. Arch Ophthalmol 1992;110(2):206-10.
96. Hoyt WF, Frisen L, Newman NM. Fundoscopy of nerve fiber layer defects in glaucoma.
Invest Ophthalmol 1973;12(11):814-29.
97. Jonas JB, Nguyen NX, Naumann GO. The retinal nerve fiber layer in normal eyes.
Ophthalmology 1989;96(5):627-32.
98. Airaksinen PJ, Drance SM, Douglas GR, et al. Visual field and retinal nerve fiber layer
comparisons in glaucoma. Arch Ophthalmol 1985;103(2):205-7.
99. Healey PR, Mitchell P, Smith W, Wang JJ. Optic disc hemorrhages in a population
with and without signs of glaucoma. Ophthalmology 1998;105(2):216-23.
100. Budenz DL, Anderson DR, Feuer WJ, et al. Detection and prognostic significance of
optic disc hemorrhages during the Ocular Hypertension Treatment Study. Ophthalmology
2006;113(12):2137-43.
101. Leske MC, Heijl A, Hyman L, et al. Predictors of long-term progression in the early
102. Uhler TA, Piltz-Seymour J. Optic disc hemorrhages in glaucoma and ocular hypertension:
implications and recommendations. Curr Opin Ophthalmol 2008;19(2):89-94.
103. Bengtsson B, Leske MC, Yang Z, Heijl A. Disc hemorrhages and treatment in the early
104. Jonas JB, Nguyen XN, Gusek GC, Naumann GO. Parapapillary chorioretinal atrophy in normal
and glaucoma eyes. I. Morphometric data. Invest Ophthalmol Vis Sci 1989;30(5):908-18.
105. Teng CC, De Moraes CG, Prata TS, et al. Beta-Zone parapapillary atrophy and the
velocity of glaucoma progression. Ophthalmology 2010;117(5):909-15.
106. Teng CC, De Moraes CG, Prata TS, et al. The region of largest beta-zone parapapillary
atrophy area predicts the location of most rapid visual field progression. Ophthalmology
2011;118(12):2409-13.
107. See JL, Nicolela MT, Chauhan BC. Rates of neuroretinal rim and peripapillary
atrophy area change: a comparative study of glaucoma patients and normal controls.
108. Jonas JB, Gusek GC, Naumann GO. Optic disc, cup and neuroretinal rim size, configuration
and correlations in normal eyes. Invest Ophthalmol Vis Sci 1988;29(7):1151-8.
109. Healey PR, Mitchell P, Smith W, Wang JJ. Relationship between cup-disc ratio and
optic disc diameter: the Blue Mountains Eye Study. Aust N Z J Ophthalmol 1997;25
Suppl 1:S99-101.
110. Heijl A,Molder H. Optic disc diameter influences the ability to detect glaucomatous disc
damage. Acta Ophthalmol (Copenh) 1993;71(1):122-9.
111. Medeiros FA, Zangwill LM, Bowd C, Weinreb RN. Comparison of the GDx VCC scanning
laser polarimeter, HRT II confocal scanning laser ophthalmoscope, and stratus OCT optical
coherence tomograph for the detection of glaucoma. Arch Ophthalmol 2004;122(6):827-37.
112. Strouthidis NG, Scott A, Peter NM, Garway-Heath DF. Optic disc and visual field
progression in ocular hypertensive subjects: detection rates, specificity, and agreement.
113. Leung CK, Liu S, Weinreb RN, et al. Evaluation of retinal nerve fiber layer progression
in glaucoma a prospective analysis with neuroretinal rim and visual field progression.
Ophthalmology 2011;118(8):1551-7.
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114. Wollstein G, Garway-Heath DF, Fontana L, Hitchings RA. Identifying early glaucomatous
changes. Comparison between expert clinical assessment of optic disc photographs
and confocal scanning ophthalmoscopy. Ophthalmology 2000;107(12):2272-7.
115. Strouthidis NG, Garway-Heath DF. New developments in Heidelberg retina tomograph
for glaucoma. Curr Opin Ophthalmol 2008;19(2):141-8.
116. Oddone F, Centofanti M, Rossetti L, et al. Exploring the Heidelberg Retinal Tomograph
3 diagnostic accuracy across disc sizes and glaucoma stages: a multicenter study.
Ophthalmology 2008;115(8):1358-65, 65 e1-3.
117. Mai TA, Reus NJ, Lemij HG. Diagnostic accuracy of scanning laser polarimetry with
enhanced versus variable corneal compensation. Ophthalmology 2007;114(11):1988-93.
118. Leung CK, Yu M, Weinreb RN, et al. Retinal nerve fiber layer imaging with spectral-
domain optical coherence tomography: patterns of retinal nerve fiber layer progression.
Ophthalmology 2012;119(9):1858-66.
119. Sung KR, Sun JH, Na JH, et al. Progression detection capability of macular thickness
in advanced glaucomatous eyes. Ophthalmology 2012;119(2):308-13.
120. Araie M. Test-retest variability in structural parameters measured with glaucoma imaging
devices. Jpn J Ophthalmol 2013;57(1):1-24.
121. Aulhorn EH, H. Early visual field defects in glaucoma. In: Leydhecker W, ed. Glaucoma
Tutzing Symposium. Basel, Switzerland 1966.
122. Morales J, Weitzman ML, Gonzalez de la Rosa M. Comparison between Tendency-Oriented
Perimetry (TOP) and octopus threshold perimetry. Ophthalmology 2000;107(1):134-42.
123. Shah NN, Bowd C, Medeiros FA, et al. Combining structural and functional testing for
detection of glaucoma. Ophthalmology 2006;113(9):1593-602.
124. Sample PA, Medeiros FA, Racette L, et al. Identifying glaucomatous vision loss with
visual-function-specific perimetry in the diagnostic innovations in glaucoma study. Invest
125. Trible JR, Schultz RO, Robinson JC, Rothe TL. Accuracy of glaucoma detection with
frequency-doubling perimetry. Am J Ophthalmol 2000;129(6):740-5.
126. van der Schoot J, Reus NJ, Colen TP, Lemij HG. The ability of short-wavelength
automated perimetry to predict conversion to glaucoma. Ophthalmology 2010;117(1):30-4.
127. Bengtsson B, Heijl A. A visual field index for calculation of glaucoma rate of progression.
Am J Ophthalmol 2008;145(2):343-53.
128. Chauhan BC, Garway-Heath DF, Goni FJ, et al. Practical recommendations for measuring
rates of visual field change in glaucoma. Br J Ophthalmol 2008;92(4):569-73.
129. Brusini P, Filacorda S. Enhanced Glaucoma Staging System (GSS 2) for classifying
functional damage in glaucoma. J Glaucoma 2006;15(1):40-6.
130. Ng M, Sample PA, Pascual JP, et al. Comparison of visual field severity classification
systems for glaucoma. J Glaucoma 2012;21(8):551-61.
131. Leske MC, Heijl A, Hyman L, Bengtsson B. Early Manifest Glaucoma Trial: design and
baseline data. Ophthalmology 1999;106(11):2144-53.
132. Mills RP, Budenz DL, Lee PP, et al. Categorizing the stage of glaucoma from pre-
diagnosis to end-stage disease. Am J Ophthalmol 2006;141(1):24-30.
133. Hodapp E, Parrish RKI, Anderson DR. Clinical decisions in glaucoma. St Louis: The CV
Mosby Co, 1993.
71
72
CHAPTER 2
Classification
and Terminology
73
74
Classification
and Terminology
2.1 - PRIMARY CONGENITAL FORMS/CHILDHOOD GLAUCOMAS
Primary congenital glaucoma is a rare disease but has a major impact on the child’s
development and quality of life over his/her whole life span. Early diagnosis and
appropriate therapy can make a huge difference in the visual outcome and can prevent
lifelong disability. Surgical treatment is always necessary1, 2 [I,C].
2.1.1 Primary congenital glaucoma (PCG): from birth to >2 years of life
(1) Neonatal or newborn onset (0-1 month)

(2) Infantile onset (>1 until 24 months)
(3) Late onset or late recognized (>2 years)
(4) Spontaneously non-progressing cases with normal IOP but typical signs of
PCG may be classified as PCG
Etiology:
Angle dysgenesis is caused by incomplete development of the trabecular meshwork
before and/or after birth. Strong monogenetic influence. Heredity shows recessive
inheritance with variable penetrance in most cases or is sporadic. Specific chromosomal
abnormalities have been identified at chromosomes 1p36 and 2q212.
Pathogenic mechanism:
De cre ase d aque ous out f low c ause s signif ic ant e levation of IOP. Isolate d
trabeculodysgenesis is the most common form of primary congenital glaucoma.
Epidemiology:
Congenital glaucoma occurs in about 1 in 12-18,000 births among Caucasians.
Incidence can be 5 to 10 times higher if consanguinity of parents is present. Severe
visual disability is common. PCG is more common in males (65%), and is bilateral in
70% of patients.
Symptoms:
Crying unhappy child during first weeks or year of life.
Not always symptomatic.
Signs:
Photophobia, tearing, blepharospasm, and eye rubbing are typical early signs.
Eyes are larger compared to age, with corneal diameter usually >10.5 mm at birth
and >12 mm in the first year of life. Axial length is increased, >20 mm at birth or >22
mm after 1 year. Corneal oedema is frequent; epithelial and stromal oedema can de
associated with ruptures of Descemet’s Membrane, or Haab’s striae, not to be confused
with forceps delivery trauma.
IOP can sometimes be measured in the awaked child with hand-held tonometers.
Under general anesthesia the level of IOP is often artificially lowered by sedation and
anesthetic medications: IOP values alone are insufficient to confirm the diagnosis
unless IOP is extremely elevated and confirmed by corneal signs. Severe cases show
75
Classification and Terminology
extremely extended globe when the diagnosis is delayed, described as “buphthalmos”

(Ox eye). A useful approach is to compare the width of the palpebral apertures.
The optic nerve head shows pressure distension or uniform cup enlargement in
newborns; cupping is a typical signs for later stages (CDR >0.3). Optic disc signs may
be reversible with the normalization of IOP.
Gonioscopy shows anterior insertion of the iris, forming a scalloped line with persistent
uveal tissue and poorly differentiated structures and/or trabeculodysgenesis often
described as Barkan´s “membrane”.
Treatment:
Initial surgery is indicated in nearly all cases with primary congenital glaucoma 2-5 [I,D].
Classical initial surgery is goniotomy or trabeculotomy1, 6-8. 360° trabeculotomy using a
catheter to open the whole circumference of Schlemm’s canal has been described with
favourable results9-11. Filtration surgery may be indicated if these are unsuccessful [I,D].
Repeat surgery is relatively frequent.
Medical treatment is usually neither effective nor practicable in the long term. Medications,
including oral CAIs can be used while decision is made on a surgical approach and
for eyes where surgery fails to achieve IOP control.2. Cycloablation is an intermediate
or add-on procedure when primary trabecular surgery has failed. Severe cases and
secondary childhood glaucomas, particularly aphakic childhood glaucoma, sometimes
need long-tube drainage device surgery.
Cases with later manifestation usually do not have enlargement of the globe and may
have a more favourable outcome with surgery.
2.1.2 Late-onset childhood open-angle glaucoma/Early Juvenile (onset >2

to puberty)
Etiology and pathophysiology:

as in PCG, except :
- no ocular enlargement
- no congenital ocular anomalies or syndromes
- asymptomatic until field loss advanced
Signs:
open angle, elevated IOP, optic nerve and visual field damage depending on the stage
of disease
Treatment:
See above 2.1.1.1
The treatment of pediatric glaucoma cases is particularly challenging due to the nature
of the disease and to the intrinsic difficulties in operating them and in examining
patients of this age. Treatment is to be adapted to the primary anomaly, and the
mechanism of IOP elevation [I,D]. Whenever possible these cases should be referred
to tertiary care centers.
76
2.1.3 Secondary Childhood Glaucoma
A variety of pathogenetic mechanisms are possible. A complete list and extensive

discussion are outside the scope of the guidelines.
2.1.3.1 Glaucoma associated with non-acquired ocular anomalies
y Axenfeld Rieger anomaly (Syndrome if systemic associations)

y Peters anomaly (Syndrome if systemic associations)
y Ectropion uveae
y Congenital iris hypoplasia
y Aniridia
y Persistent fetal vasculature/PFV (if glaucoma present before cataract surgery)
y Oculodermal melanocytosis (Nevus of Ota)
y Posterior polymorphous dystrophy
y Microphthalmos
y Microcornea
y Ectopia lentis
2.1.3.2 Glaucoma Associated with Non-acquired Systemic Disease or Syndrome
y Chromosomal disorders such as Trisomy 21 (Down syndrome)
y Connective tissue disorders

o Marfan syndrome
o Weill-Marchesani syndrome
o Stickler syndrome
y Metabolic disorders
o Homocysteinuria
o Lowe syndrome
o Mucopolysaccharidoses
y Phacomatoses
o Neurofibromatosis (NF-1, NF-2)
o Sturge-Weber syndrome
o Klippel-Trenaunay-Weber syndrome
o Rubinstein-Taybi
o Congenital rubella
2.1.3.3 Glaucoma Associated with Acquired Condition
y Uveitis
y Trauma (hyphema, angle recession, ectopialentis)
y Steroid induced
y Tumors (benign/malignant, ocular/orbital)
y Retinopathy of Prematurity
77
2.1.3.4 Glaucoma Following Childhood Cataract Surgery
Secondary glaucoma is a frequent serious complication after cataract surgery in early

infancy. The incidence may increase up to 50% if cataract surgery is performed before
the 9th month of life12, 13. This secondary glaucoma is difficult to treat and often needs
long-tube drainage device surgery for long-term IOP control.
2.1.3.5 Treatment of secondary childhood glaucoma [I,D]
The management of these cases is particularly challenging.

Medical treatment is usually not effective nor practicable in long term. Medications,
including oral CAIs can be used while decision is made on a surgical approach and in
case of failed surgery while awaiting for further options.
Primary surgery: early goniotomy or trabeculotomy or filtration surgery may be indicated
if these are unsuccessful. Repeat surgery is relatively frequent.
Treatment to be adapted to the primary anomaly, the mechanism of IOP elevation and
the quality of life of the patient. These cases require highly specialized care.
78
2.2 - PRIMARY OPEN-ANGLE GLAUCOMAS

The open-angle glaucomas are chronic, progressive optic neuropathies, that have in
common characteristic morphological changes at the optic nerve head and retinal nerve
fibre layer in the absence of other ocular disease or congenital anomalies. Progressive
retinal ganglion cells death and visual field loss are associated with these changes.
2.2.1 Epidemiology
Glaucoma is the second leading cause of blindness both in Europe and worldwide. It
is the most frequent cause of irreversible blindness. POAG is unusual under the age of
50 yrs. Its prevalence increases with age14-25. However, the reported percentage largely
depends on definition.
2.2.2 Risk factors for open-angle glaucoma
As most population studies did not differentiate between POAG and secondary open
angle glaucomas such as pseudoexfoliation (PEX) glaucoma, the following statements
apply to both varieties, here are labelled OAG.
• Risk assessment
Consideration of risk factors is important: it helps to identify individuals who can be
targeted for early detection and to guide management decisions about the initiation
and escalation of treatment in established glaucoma patients.
• Terminology
Risk Factors: risk factors for open-angle glaucoma (OAG) are those statistically
associated with the development of OAG or conversion from ocular hypertension to
glaucoma26.
Prognostic Factors: prognostic factors for OAG are statistically associated with the
progression of established OAG. Neither risk factors nor prognostic factors establish
causation. Sometimes the terms risk factors and prognostic factors are used
interchangeably.
Predictive Factors: the term predictive factors should be used for factors which are
associated with increased risk for glaucoma and which are part of the definition of
OAG, such as optic disc parameters and visual field indices.
79
2.2.2.1 Risk factors for the development of OAG (See FC V)
Initial evidence on potential risk factors for OAG has been provided by cross-sectional
population-based studies. Firm conclusions on risk factors for the development of OAG can
only be drawn by longitudinal population-based cohort studies27-30.
a) Age
Cross-sectional population-based studies have consistently reported that
the prevalence of OAG increases dramatically with age14-17,19-25,31. Longitudinal
population-based studies have confirmed that older age is an important risk
factor for OAG27-30. Two studies reported a 6% and 4% increased risk per year
of age at baseline of developing OAG.
b) Intraocular pressure (IOP)

Higher IOP has been consistently associated with the prevalence14-17,19-25,31 and
incidence of OAG27,28,30,32. According to longitudinal data, the risk of developing
OAG increases by 11-12% in Caucasians27,28, 10% in people of African origin32
and 18% in Latinos30 for each 1 mmHg increase in IOP. To date, IOP is the only
modifiable risk factor for OAG.
c) Race/ethnicity
The prevalence of glaucoma is several times higher in African-Americans and
Afro-Caribbeans than in Caucasians18,33,34. In Latinos, it has been shown that the
prevalence20-23 and incidence35 of OAG is higher than in Caucasians, but lower
than in Afro-Caribbeans.
d) Family history of glaucoma

Two studies studying different ethnic groups found that the risk of having OAG
was 9.2-fold and 4 fold higher, respectively for individuals having a first-degree
relative with confirmed OAG, compared with those who did not 36, 37. Also, self–
reported family history of glaucoma has been associated with increased risk of
developing OAG27,29.
e) Pseudoexfoliation
Population-based studies which specifically assessed pseudoexfoliation and
pseudoexfoliative glaucoma have consistently reported that pseudoexfoliation is
associated with increased prevalence of OAG19,24,38-47. Based on longitudinal data,
the presence of pseudoexfoliation is associated with an 11.2-fold increased risk
of developing OAG27.
f) Central corneal thickness (CCT)

In two population based studies, there was a 41% and 30% increased risk of
developing OAG per 40 μm thinner CCT29,48.
g) Myopia
Several cross-sectional population-based studies identified moderate to high
myopia (greater than -3 diopters) as a factor associated with increased OAG
80
prevalence 47,49-55 . A Dutch study showed that subjects with high myopia
(greater than -4 D) had a 2.3-fold increased risk for developing OAG28. Latinos
in California had a risk of OAG increased by 48% with each 1 mm increase
in axial length30.
h) Ocular perfusion pressure

The association of low ocular per fusion pressure with increased OAG
prevalence has been a consistent finding in population-based studies20,31, 56-61.
Recent evidence suggests that this association may depend on whether
subjects are treated for systemic hypertension or not29,56,58,61-66.
A phenotype characterized by vascular dysregulation has been described 64.
The Barbados Eye Study confirmed that low ocular perfusion pressure
increases the risk for the development of OAG29.
Because of our limited understanding of this complex variable and of its
interaction with potential risk factors for glaucoma, the exact place of ocular
perfusion pressure in glaucoma management remains unclear 67-69.
i) Other factors
There have been reports on other factors that may be associated with increased
risk for OAG, such as diabetes, systemic blood pressure, migraine, Raynaud
syndrome and obstructive sleep apnoea. However, data from the literature are
inconsistent.
j) Risk factors by type of OAG

In general, population-based studies analyses have not dif ferentiated
between types of OAG. A recent analysis which considered POAG and PEX
glaucoma revealed that IOP was the only factor associated with both of
them; vascular systemic diseases and their treatment were associated only
with POAG47. This may suggest differences in pathogenesis between these
two common types of OAG.
2.2.2.2 Risk factors and predictive factors for the conversion of ocular hypertension
to POAG
The Ocular Hypertension Treatment Study (OHTS), and the European Glaucoma
Prevention Study (EGPS)70 are two randomized controlled trials (RCTs) which evaluated
the effect of IOP-lowering treatment on the conversion of ocular hypertension to POAG.
The following risk factors and predictive factors were consistently reported in both the
OHTS and the EGPS:
% Age (risk increased by 26% per decade)

% IOP (risk increased by 9% per 1 mmHg)
% Vertical and horizontal cup-to-disc ratio (risk increased by 19% per 0.1 larger)
% Pattern standard deviation (PSD) in the visual field (risk increased by 13% per
0.2 dB greater)
% CCT (2.04 fold increased risk per 40 μm thinner)
81
Based on the pooled OHTS–EGPS predictive model, a quantitative calculator was

developed to estimate the 5-year risk for the conversion of ocular hypertension to
POAG71. This tool is available to the clinician and may help to discuss frequency of
visits and possible treatment.
However, limitations should also be considered. Because the calculator was based
on the OHTS and EGPS data sets, results may not apply to individuals < 40 years
old, individuals who have untreated IOPs < 22 mmHg or who are not of Caucasian
or of African origin. Also, the calculator does not take into account other factors
associated with increased risk for glaucoma, such as family history of glaucoma and
pseudoexfoliation. In addition, life expectancy issues should be addressed.
2.2.2.3 Prognostic factors for progression of OAG
Factors associated with the progression of established OAG have been identified by
large RCTs: Early Manifest Glaucoma Trial (EMGT)72, Advanced Glaucoma Intervention
Study (AGIS)73, Collaborative Initial Glaucoma Treatment Study (CIGTS)74, Collaborative
Normal Tension Glaucoma Study (CNTGS)75.
a) Age
Older age is significantly associated with increased risk for the progression
of OAG. In the EMGT, after a mean follow-up of 8 years, patients ≥ 68 years
old had a 51% increased risk of progression compared to those who were
younger72. In the AGIS the risk of progression increased by 30% with every 5
years increase in age73; in CIGTS the risk increased by 35% for every decade74.
Also, in the untreated arm of the EMGT, progression was considerably faster
in older than in younger patients76.
b) IOP
Most of the above RCTs suggest a positive effect of IOP reduction on the onset
or progression of glaucomatous damage. In the EMGT the risk of progression
decreased by about 10% with each mmHg of IOP reduction from baseline
to the first follow-up visit77. Conversely, the role of long term IOP fluctuation
in glaucoma progression is still debated 78-80. Also, the role of diurnal IOP
fluctuation in glaucoma progression needs to be investigated more thoroughly
in RCTs.
c) Pseudoexfoliation
In the EMGT, the risk of progression increased by a 2.12-fold in those with
pseudoexfoliation compared with those without pseudoexfoliation72. In addition,
in the untreated arm of the EMGT, progression was considerably faster in
eyes with pseudoexfoliation, despite similar baseline IOP values between the
pseudoexfoliative and non pseudoexfoliative eyes76. Pseudoexfoliation has not
been evaluated in the AGIS, CIGTS and CNTGS.
d) CCT
In the EMGT, thinner CCT was a significant but weak prognostic factor for OAG
82
and this association was observed only in patients with higher baseline IOP72.
The role of CCT in glaucoma progression has not been evaluated in the AGIS,
CIGTS and CNTGS.
e) Disc haemorrhages
In the CNTGS the presence of optic disc haemorrhages was significantly
associated with glaucoma progression80. Also, in the EMGT patients with disc
haemorrhages had significantly shorter time to progression81. A systematic review
(January 1950-January 2013) evaluating risk factors for glaucoma among routine
diagnostic examination reported disc haemorrhage (LR, 12; 95% CI, 2.9-48)
being highly suggestive of glaucoma, but the absence of a haemorrhage was
nondiagnostic (LR, 0.94; 95% CI, 0.83-0.98)82.
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83
2.2.3 Primary Open-Angle Glaucoma
Definition:
Primary open-angle glaucoma (POAG) is a chronic progressive optic neuropathy with
characteristic morphological changes at the optic nerve head and retinal nerve fibre
layer in the absence of other ocular disease or congenital anomalies. Progressive retinal
ganglion cell death and visual field loss are associated with these changes.
Etiology:
The etiology of primary open angle glaucoma remains unclear. Multiple genetic factors
and the influence of co-morbidities are likely to play a role.
Pathophysiology:
The current concept of how damage is elicited includes deformation of the lamina cribrosa
caused by IOP levels that are not tolerated by the individual eye. This is thought to result in
axonal damage with consequent apoptotic death of the retinal ganglion cells. A substantial
proportion of patients develop POAG at IOPs within the normal range. Any increase in IOP
is caused by elevated outflow resistance in the trabecular meshwork outflow pathways.
Treatment:
POAG is treated by reducing intraocular pressure using medication, laser or incisional
surgery (See Ch 3). So far, there is no evidence for other suggested treatment modalities,
e.g. neuroprotection or modifying blood flow.
2.2.3.1 Primary Open-Angle Glaucoma / High Pressure Glaucoma (POAG/HPG)
The relative risk for POAG rises continuously with the level of the intra-ocular pressure
(IOP), and there is no evidence of a threshold IOP for the onset of the condition. It is
presumed that risk factors other than IOP have a relatively greater importance if there is
glaucomatous optic neuropathy at the lower (statistically ‘normal’) pressure levels. POAG
has been arbitrarily subdivided into High Pressure and Normal-Pressure disease to
reflect this, even though they may represent a spectrum of optic neuropathies variably
sensitive to the IOP. See Ch. Introduction.
Etiology:
Unknown
Pathomechanism:
Unknown.
TIGR and Myoc mutations may be associated83, 84.
Features:
% Onset: from the young adult age onwards
% Signs and symptoms:
o Asymptomatic until field loss advanced
o Elevated IOP without treatment (diurnal tension curve)
84
% Optic nerve head: acquired characteristic glaucomatous damage and/or retinal

nerve fiber layer changes (diffuse or localized defects) (See Ch. 1)
% Visual field: usually detectable glaucomatous defects corresponding to the optic
disc damage may be present
% Gonioscopy: open anterior chamber angle (not occludable, no goniodysgenesis).
(See Ch. 1).
Treatment:
Refer also to Introduction II and Ch. 3
A target pressure is to be identified for each case (See also Ch. 3.2 and FC IX-X) [I,D].
a) Medical treatment (See FC XI-XIII)
1. Mono therapy
2. Combination therapy as needed in selected patients
b) Laser trabeculoplasty (LTP)
c) Filtration Surgery with / without antimetabolites
d) Adjunctive medical therapy when needed
e) Insertion of aqueous long- tube drainage implants
f) Cyclodestructive procedures
Choice of primary therapeutic modality needs to be made on an individual patient

basis [I,D].
Laser trabeculoplasty can be considered as primary treatment and as an alternative to
additional medications [I,A].
2.2.3.2 Primary Open-Angle Glaucoma / Normal–Pressure Glaucoma (POAG/NPG)
Etiology:
Unknown
Pathomechanism:
Unknown.
Optineurin mutation has been found in families with NPG
Features:
% Onset: from the 35th year onwards
o Normal IOP without treatment (diurnal curve or 24-hour phasing). Asymptomatic
until field loss advanced
o Optic nerve head damage typical of glaucoma
o Disc haemorrhages
% Visual field defects typical of glaucoma; e.g. paracentral defects
% Gonioscopy: open anterior chamber angle (exclude intermittent angle-closure; See Ch. 2)
% No history or signs of other eye disease or steroid use.
% Consider central corneal thickness if findings do not match; CCT may be thinner
than average (See Ch. 1.1).
85
Treatment:
Refer also to Chapter Introduction II, Ch. 3 and FC VI
There are few prospective clinical trials indicating clearly the advantages of treatment [I,A].
Target pressure: in most cases a peak IOP = 8 mm - 15 mm Hg on diurnal curve or a
30% IOP reduction from baseline (See Ch. 3.2) [I,D]
a) Medical therapy:
I. Any drug singly or in combination which is effective and tolerated,
whose IOP lowering effect is sufficient to reach a maintain the target
IOP [I,D]
II. Avoid medications with potential vasoconstrictive effects or with
systemic hypotensive effects [II,D]
III. Oral calcium channel blockers are being investigated in selected
patients by some investigators.
b) Laser trabeculoplasty [I,D]
c) Glaucoma Surgery:
In cases of progressive glaucomatous damage, in spite of maximal medical
therapy or laser trabeculoplasty, or failure to reach target pressure [I,D].
Intensive postoperative care with bleb manipulation may be needed to
maintain low IOPs [I,D]
Follow-up intervals, depending on the stage of disease and on the rate of progression,
with examination of [II,D]:
Optic disc
Visual field
IOP
ONH and RNFL documentation
2.2.4 Primary Juvenile Glaucoma
% Etiology: Unknown
% Pathomechanism: Decreased aqueous outflow
% Features:
o Onset: beyond infancy, usually after puberty or early adulthood. Heredity:
if familiar frequently dominant trait. Genes associated with primary juvenile
glaucoma have been identified as MYOC and CYP1B1
o Signs and symptoms:
No enlargement of the globe
Asymptomatic until field loss is advanced
Elevated IOP without treatment (diurnal tension curve)
Optic nerve head and RNFL: Diffuse damage typical, but any type of
glaucomatous damage
Visual field: glaucomatous defects
G onioscopy: wide open anterior chamber angle, of ten poorly
differentiated
No congenital or developmental anomalies
86
Treatment [I,D] (See FC VI):
a. Medical therapy: any ef fective and well tolerated topical regimen.

Pilocarpine causes fluctuating myopic shift, visual symptoms and headache
particularly in the young and should be avoided.
b. Surgery: early surgery often required filtering procedure or trabeculotomy;
consider antimetabolites.
c. Laser trabeculoplasty: not recommended due to poor and short-lived IOP
lowering effect.
2.2.5 Primary Open-Angle Glaucoma Suspect (POAG)
Etiology:
Unknown
Pathomechanism:
Unknown
Features:
% Visual field and/or optic disc and/or nerve fiber layer normal or suspicious,
with at least one being suspicious
% IOP can be normal or increased
Treatment [II,D] (See FC VI):

Risks and benefits of treatment need to be weighed against the risk of the development
of glaucomatous disc damage. The risk of developing glaucoma increases with the
number and strength of risk factors.
The indication for any form of therapy is relative
a) Medical therapy: any topical agent alone or in combination as long as well

tolerated and effective
b) Avoid adjunctive medical treatment unless strictly needed
c) Laser trabeculoplasty: not usually indicated
d) Filtering operation: not indicated
e) Follow-up [II,D] at intervals of 6-12 months initially, to be increased if all
parameters remain normal with examination of:
I. Optic disc
II. Visual field
III. IOP
IV. ONH RNFL documentation initially and every 2-3 years
87
2.2.6 Ocular Hypertension (OH)
Etiology:
Unknown
Pathomechanism:
Unknown
Features:
o IOP > 21 mm Hg without treatment
o Visual field: normal
o Optic disc and retinal nerve fibre layer: normal
o Gonioscopy: open anterior chamber angle (exclude intermittent angle-closure.
See Ch 2.4.2.2)
o No history or signs of other eye disease or steroid use.
% Other risk factors: none
FC VI - Treatment Options
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88
Treatment:
Although in the past it has been used as a diagnosis, Ocular Hypertension should be
used to indicate that the IOP is consistently outside 2 or 3 standard deviations above
the mean. Consider corneal thickness (See Introduction II and Ch. 1.1; FC II and IV).
A modest increase in IOP is not sufficient reason for treatment, but consider it in
patients with repeated IOPs in the high twenties, even without risk factors. For treatment
modality See Ch. 4.2.3-a (See also Ch. 2.2.3. and flow-charts).
% If left untreated (See Ch. Introduction II)

o up to 9.5% develop glaucoma over 5 year of follow-up
o the risk of developing glaucoma increases with increasing IOP
o prophylactic IOP-lowering therapy to be discussed with individual patients
considering the presence of risk factors
o Follow-up [II,D] at intervals of 12-24 months initially, to be increased if all

parameters remain negative, with examination of:
Optic disc
Visual field
IOP
ONH and RNFL photographs initially and every 2-3 years
Patients for the ocular hypertension treatment study (Ch. Introduction II) were selected
excluding myopes, labile diabetics, poor compliance. In most of Europe black Africans
are a minority.
Assess each patient individually when deciding whether or not to treat [I,D].
89
2.3 - SECONDARY GLAUCOMAS

Secondary glaucomas are a heterogeneous group of conditions, in which elevated
IOP is the leading pathological factor causing glaucomatous optic neuropathy.
Most forms of secondar y glaucoma like uveitic or traumatic glaucoma have
complex pathomechanisms including both an open or closed angle.
2.3.1 Secondary Open-Angle Glaucoma
2.3.1.1 Secondary Open-Angle Glaucomas Caused By Ocular Disease
2.3.1.1.1 Exfoliative (pseudoexfoliative) glaucoma
Features:
% Onset: usually older than 60 years
% Asymptomatic until visual field loss advanced
% One or both eyes affected, often bilateral and asymmetrical
Etiology and pathogenic mechanisms.

Exfoliative glaucoma (XFG) develops from exfoliation (pseudoexfoliation) syndrome
( XFS), in which an abnormal fibrillo-granular protein (ex foliation material) is
produced in the eye and the body. Development of XFS is strongly associated
with certain variants of the LOXL1 gene, but the onset of glaucoma may depend
on other environmental and/or genetic factors. In the eye exfoliation material
accumulates in a characteristic pattern on the anterior lens capsule, pupillary
margin, trabecular meshwork and the zonules 85, 86 . Pigment granules from the
posterior layer of the iris are liberated and together with the exfoliation material
play an impor tant role in the development of decreased aqueous humour
outflow and elevation of IOP, which may lead to the development of glaucoma.
Clinically both XFS and XFG may appear in only one eye, but they may develop
gradually in the fellow eye in many cases. To identify exfoliation material pupil
dilation is recommended. Typically XFG develops after 60 years of age, the IOP
is considerably higher than that in POAG, and the diurnal IOP fluctuation is high.
As a consequence, in the involved eye(s) optic nerve head damage and visual
field deterioration are frequently severe already at the time of the first visit. At a
population level, this may partially be counterbalanced by the fact that in certain
countries XFG is significantly less undiagnosed than POAG 87. In XFG the risk
for progression is particularly high even when the eye is under IOP lowering
treatment76 . XFS and XFG are associated with poor pupil dilation and other
ocular alterations like dense nuclear cataract and zonular damage which make
cataract surgery more difficult and increase the risk for surgical complications 86.
Due to zonular damage lens dislocation and resulting secondary angle closure
may occur.
90
Epidemiology:
XFG is the most common type of secondary open angle glaucomas, its prevalence
varies considerably across populations24, 86. According to population-based data, XFG
develops in approximately 15% to 26% of eyes with XFS (depending on the definition of
glaucomatous damage) over a 5 year period27.
Also, it has been reported that XFS and XFG are associated with systemic diseases,
particularly cardiovascular alterations88. However, there are recent reports which do not
support this association47, 61, 89-91.
Signs and symptoms:

IOP: > 21 mm Hg, frequently higher than in average POAG cases.
Visual field loss as in POAG; frequently severe at least in one eye.
Dandruff-like exfoliation material on the pupil border and on the surface of the anterior
lens capsule except the central zone, better visualized after pupillary dilation. The
pupillary collarette is irregular and typically has a moth-eaten appearance.
Pigmentary loss from the central or mid-iris and positive transillumination are possible.
The angle can be open, narrow or closed; usually the TM is heavily pigmented with a
blackish hue and dandruff-like particles and pigment granules may be seen in the lower
angle recess.
When pigment accumulates along an ondulating line on or anterior to the Schwalbe’s
line, this feature is called Sampaolesi’s line, which is pathognomonic of XFS.
Loose zonules are frequent with occasional phacodonesis, lens subluxation and more
frequent complications during cataract surgery.
Narrow or closed-angle is relatively common.
Treatment:
Decrease the IOP with all medications, laser trabeculoplasty and filtering surgery used
in the treatment of POAG. Usually XFG responds well to laser trabeculoplasty 92 To
achieve target IOP usually more medications are needed than in POAG. Due to the
high diurnal IOP fluctuation, to characterize untreated baseline IOP and IOP under
treatment several IOP measurements are necessary. When XFG is clinically unilateral
the fellow eye must be also carefully followed because there is a high probability of
development of XFG93.
2.3.1.1.2 Pigmentary glaucoma
Etiology:
Melanin granules cause an increase of trabecular meshwork outflow resistance and
hence an elevation of IOP. The current understanding is that trabecular meshwork cells
phagocytise pigment, which subsequently leads to their death94.
Melanin pigment is released from the iris pigmented epithelium as the result of
rubbing between lens zonules and posterior surface of the iris. Posterior bowing of
the iris with “reverse pupillary block” configuration is noted in many eyes with pigment
dispersion95,96.
91
Three entities can be described:

% Pigment dispersion syndrome (PDS) - ocular condition, usually bilateral
characterized by dispersion of iris pigment
% Pigmentary ocular hypertension (POH) - pigment dispersion syndrome with
elevated IOP and without glaucomatous optic neuropathy
% Pigmentary glaucoma (PG) - glaucomatous optic neuropathy and pigment
dispersion syndrome
Epidemiology:
PG represents 1-1.5% of all glaucoma cases97. It is more common in Caucasian myopic
men. It typically diagnosed at the age of 30-50 years. The risk of developing glaucoma
in patients with PDS is 25 - 50%.
The estimated incidence of PDS and PG is 4.8/100 000 and 1.4/100 000 population per
year respectively. The risk of developing pigmentary glaucoma from pigment dispersion
syndrome is 10% at 5 years and 15% at 15 years98.
Symptoms:
Patients may experience transient visual blurring or halos during episodes of IOP rise,
particularly after exercise or pupillary dilation, uncommonly associated with mild to
moderate pain.
Signs:
PDS maybe either unilateral or bilateral. Signs of PDS or PG are very deep anterior
chamber with backward bowing of the peripheral iris, midperipheral iris transilluminations
with a radial spoke like pattern due to pigment loss best visible with retroillumination,
pigment deposition on the iris surface and lens equator among zonular insertions,
pigment deposition in the corneal endothelium typically accumulating vertically as a
Krukenberg spindle. The presence of Krukenberg spindle is not necessary to make
the diagnosis of PDS and may occur in other conditions such as exfoliation syndrome.
Gonioscopy shows a homogenously dark brown, densely pigmented trabecular
meshwork around 360° and pigment at or anterior to the Schwalbe's line, not to be
confused with the Sampaolesi’s line of pseudoexfoliation; dim light in the examination
room is recommended in order pupillary constriction and enhance gonioscopic
observation of peripheral iris shape. Ultrasound biomicroscopy (UBM) can be helpful
to confirm reverse pupillary block. PDS and PG can be independently combined with
primary angle closure.
IOP is typically elevated with large fluctuations. Gradual decrease of IOP after 60 years
of age has been reported99.
Treatment:
yMedical treatment recommendations for PG are not different to that of POAG
[I,D]. Pilocarpine is no longer a preferred drug, but if used, one should check the
peripheral retina for tears [II,D].
yLaser trabeculoplasty [I,C] is effective. However, the heavily pigmented trabecular
meshwork warrants power settings lower than usual [I,D]. The initially good
pressure fall may be lost over time. Repeat ALT is rarely successful100. c) Nd:YAG
laser peripheral iridotomy (LPI) has been proposed as a means for eliminating
92
reverse pupillary block (if present). The benefit from an LPI in patients with PDS
and pigmentary ocular hypertension is not established101. d) Filtering procedures
[I,D] are usually as successful as in POAG. Young myopic patients are at
increased risk of hypotony maculopathy102.
Examination after exercise should be considered, especially when visual symptoms
after exercises are reported. Increased pigment dispersion with posterior iris bowing
during exercise is a sign of potentially progressing disease; in such patients; LPI may
be considered103.
2.3.1.1.3 Lens-induced open-angle glaucoma
Etiology:
In lens induced open angle glaucoma trabecular meshwork outflow pathways are
obstructed by lens particles and/or inflammatory cells104.
yPhacolytic glaucoma: the trabecular meshwork is obstructed by lens material
leaking from mature or hypermature cataract
yTraumatic lens injury: the trabecular meshwork is obstructed by lens particles
from a traumatically or surgically injured lens
yPhacoanaphylactic glaucoma: lens proteins lead to granulomatous uveitis affecting
the trabecular meshwork.
ySympathetic Ophthalmia: in rare cases uneventful cataract surgery in one eye
can induce inflammation of the previously healthy contralateral eye leading to
IOP spikes
Clinical features:
Patients usually suffer from unilateral pain with redness and inflammation. Reduced
vision and elevated IOP. Signs of injured lens and/or mature/hypermature cataract
or cataract surgery are present, with or without iritis (cf aqueous flare and keratic
precipitates).
Treatment:
Extraction of lens or lens fragments followed by topical anti-inflammatory medication,
vitrectomy if needed [I,D].
2.3.1.1.4 Glaucoma associated with intraocular haemorrhage
Etiology:
Either acute bleeding in the anterior chamber or long standing blood in the vitreous
of any source can cause IOP elevation. Sickle cell trait / disease should always be
considered because these patients may be at a higher risk for elevated IOP.
Large quantity of normal red blood cells (hyphaema) or haemoglobin-laden macrophages
93
(haemolytic glaucoma) or degenerated red blood cells (ghost cell glaucoma) obstruct
the trabecular meshwork.
Symptoms:
Pain and eye irritation.
Signs:
Elevated IOP is more common with larger hyphaemas and is more often due to
recurrent haemorrhage or re-bleeding. Re-bleeding can follow traumatic hyphaema,
usually after 3-7 days (incidence 5 - 10%). Patients with sickle cell disease / trait
have an increased incidence of elevated IOP. They are also more prone to developing
glaucomatous neuropathy and can be more difficult to treat105.
In haemolytic glaucoma red-tinged cells in the aqueous humour and reddish brown
discoloration of the trabecular meshwork are present. “Ghost cells” occur 1 to 4 weeks
after vitreous haemorrhage and reach the anterior chamber. Small khaki-coloured
cells may be seen circulating in anterior chamber. Gonioscopic examination may show
layering of the ghost cells over the inferior part of trabecular meshwork.
Treatment:
y Topical and systemic IOP lowering medication as needed [I,D]. It is recommended
to avoid carbonic anhydrase inhibitors and hyperosmotic agents in patients with
sickle cell disease.
y Conservative treatment, bed rest, topical cycloplegics and steroids, can be
considered for uncomplicated hyphaema [II,D]. Antifibrinolytic agents such as
tranexamic acid can reduce the risk if re-bleeding106. However it is not clear
whether any of the interventions have an effect on visual acuity107.
y Wash-out through a paracentesis of the anterior chamber [II,D] and/or vitrectomy
for removing RBCs from vitreous if IOP remains high with the risk of causing
corneal blood staining and/or optic neuropathy [II,D].
2.3.1.1.5 Uveitic glaucoma
Etiology:
Acute IOP elevation is typical in Posner-Schlossman syndrome or in viral infection such
as HSV and VZV. Chronic IOP elevation is typical for Fuchs’ uveitis, juvenile idiopathic
arthritis, Behcet disease, pars planitis, sympathetic ophthalmia, sarcoidosis and syphilis.
Obstruction and oedema of the trabecular meshwork are caused by inflammatory cells,
precipitates, debris, secondary scarring and neovascularization of the chamber angle.
Secondary angle-closure glaucoma can be due to synechial closure of the chamber
angle or seclusio pupillae with subsequent appositional angle closure. Corticoid
treatment can also contribute to IOP elevation108.
Symptoms:
Pain, redness, photophobia, decreased vision are possible.
94
Signs:
Features depend on the underlying cause. Elevated IOP; some forms are associated
with wide oscillations or periodic rise in IOP.
Treatment [I,D]:
yTopical and systemic anti-inflammatory therapy according to the underlying
disease
yTopical and systemic IOP lowering medication
o traditionally topical `-blockers and CAIs were used as first-line treatment.
o prostaglandin analogues are used as first-line therapy in eyes with
controlled uveitis. There are studies that support the efficacy and safety of
prostaglandin analogues as IOP lowering medication in uveitic glaucoma109.
y Glaucoma surgery suited for the type of inflammatory disease, ALT and SLT
should be avoided110,111.
2.3.1.1.6 Neovascular Glaucoma

(See Secondary Angle Closure Glaucoma)
2.3.1.1.7 Glaucoma due to intraocular tumour
Etiology:
Reduced aqueous humour outflow due to primary or secondary intraocular tumours,
mainly of the anterior segment.
Infiltration of the trabecular meshwork by the tumour or tumour cells floating in the
aqueous humour. Trabecular meshwork obstruction due to tumour related inflammation,
tumour debris, haemorrhage or pigment dispersion. Secondary angle closure glaucoma
may also develop112.
Symptoms and signs:

Elevated IOP. A highly variable clinical picture, combining evidence of both tumour and
glaucoma.
Treatment [I,D]:
y Treatment of underlying tumour (irradiation, surgical tumour excision, enucleation)
y Topical and systemic IOP lowering medication; medical therapy is often first-line
treatment while awaiting definitive treatment:
o topical `-blockers, _-agonists, topical and systemic CAIs are safe and
effective
o prostaglandin analogues (increasing uveoscleral outflow) and
pilocarpine (increasing trabecular outflow) may theoretically promote
metastasis
y Cycloablation
y Incisional glaucoma surgery indicated only after successful tumour therapy.
95
2.3.1.1.8 Glaucoma associated with retinal detachment
Etiology and pathogenic mechanism:

Long standing retinal detachment that leads to ischaemic neovascularization. Retinal
detachment is usually associated with a reduction of IOP. Gas tamponade can elicit
significant IOP spikes. Dispersed silicon oil may cause chronic IOP elevation.
The trabecular meshwork may be obstructed by neovascularization caused by proliferative
retinopathy, or by scarring, pigment dispersion and inflammation, or by cellular debris
from retinal cells outer segments (Schwartz’s syndrome). Surgery for retinal detachment
can also cause glaucoma113.
Symptoms and signs:

Elevated IOP and retinal detachment are present. Redness and pain are common
features.
Treatment [I,D]:
ySurgery for retinal detachment
yConsider glaucoma surgery
2.3.1.2 Open-angle glaucoma due to ocular trauma
Ocular trauma leads to glaucoma by several different mechanisms. The secondary

traumatic glaucomas can be caused by both open-angle and angle-closure mechanisms.
In order to identify and treat the causes of IOP elevation; careful evaluation of the ocular
damage must be performed.
Etiology:
Blunt non-penetrating or penetrating trauma to the eye.
Pathogenic mechanisms:
Blunt non-penetrating trauma can lead to reduced trabecular outflow due to traumatic
changes of the trabecular meshwork. Scarring and inflammation of the trabecular
meshwork, obstruction by red blood cells and debris, angle recession, lens-induced
glaucoma. Elevated IOP may occur a very long time after the trauma. Positive steroid
response after anti-inflammatory treatment should also be considered. Penetrating injury
may damage one or more intraocular structure leading to elevated IOP114.
Symptoms and signs:

Redness, pain, decreased vision with acute IOP elevation, or no symptoms with chronic
IOP elevation. Acute or late IOP elevation (occurring months or even decades later) may
follow blunt trauma.
Chemical burns, hyphaema, traumatic cataract, uveitis, angle recession, ruptured iris
sphincter, iridodialysis can be present in various combinations.
Note: It is not recommended to perform gonioscopy in fresh ocular trauma to avoid
compressing the eye. This examination can be delayed for several weeks.
96
Treatment [I,D]:
yAnti-inflammatory
yLong-term IOP follow up in the presence of permanent anterior segment damage.
yGlaucoma surgery
2.3.2 Iatrogenic Secondary Open-Angle Glaucomas
2.3.2.1 Glaucoma due to corticosteroid treatment
Etiology:
Topical, intravitreal as well as high dose and long-term systemic corticosteroid therapy
can induce acute or chronic IOP elevation115. The risk of IOP elevation depends on the
chemical structure (strength) of the steroid, dose, frequency and duration of therapy,
and route of administration. The risk factors for being steroid responder are: POAG,
family history of glaucoma, diabetes, myopia, rheumatoid arthritis, children and elderly
patients.
Corticosteroids induce changes in the trabecular extracellular matrix (glycoproteins)
which lead to decreased outflow facility. A TIGR gene modification is present116.
Symptoms:
Pain and eye irritation are possible but not at all mandatory especially in acute IOP
elevation.
Signs:
Elevated IOP usually develops 2 to 6 weeks after initiating therapy, but may occur
at any time. Usually IOP elevation is slowly reversed after stopping the use of
corticosteroid. Corneal oedema can be present. Prolonged IOP elevation can lead to
typical glaucomatous optic nerve head changes and visual field damage.
Treatment [I,D]:
yDiscontinuation of corticosteroid therapy is recommended; steroid-sparing
therapy of underlying condition should be considered. If this is not possible,
consider switching to weaker steroid (e.g. loteprednol, fluorometholone)
yLaser trabeculoplasty
yGlaucoma surgery may be performed in intractable cases
2.3.2.2 Secondary open-angle glaucoma due to ocular surgery and laser
Ocular surgery can cause secondary open-angle glaucoma by some of the mechanisms
discussed above: intraocular haemorrhage, inflammatory reaction, lens material,
pigmentary loss from uveal tissue, or trauma117.
97
Open-angle glaucoma following ocular surgery or laser is a result of reduced trabecular
outflow:
yIOP elevation after intraocular surgery is usually transient. The elevated IOP
may be caused by: viscoelastic material, inflammatory debris, vitreous in
the anterior chamber after cataract surgery, lens particles, intra-operative
application of _-chymotrypsin, and prostaglandin release.
yAcu te o nset se c o nd a r y IO P e l evatio n af te r N d:YAG l a se r ir id oto my,
capsulotomy and laser trabeculoplasty. IOP elevation is usually transient,
within the first 24 hours, most frequent in the first 4 hours after treatment.
yI O P e l evati o n w i th o p e n -a n g l e fo l l ow i n g v i tre c to my w i th s i l i c o n o i l
implantation develops as a result of:
o Migration of silicon oil into anterior chamber and obstruction of the
trabecular meshwork (early post-op IOP increase) usually due to
overfill of oil.
o Migration of emulsified silicon oil into anterior chamber with obstruction
of trabecular meshwork where oil particles are partially phagocytised
by macrophages and accumulate in the trabecular meshwork especially
in the upper quadrant and can induce trabeculitis (intermediate and
late onset IOP increase). Prolonged contact of silicon oil with the
trabecular meshwork may cause permanent structural changes. Risk
factors for developing IOP elevation following vitrectomy with silicon
oil implantation include pre-existing ocular hypertension or glaucoma,
diabetes mellitus, and aphakia (closed angle type)118,119.
yUveitis-glaucoma-hyphema (UGH) syndrome - IOP elevation associated
with an anterior chamber intraocular lens due to induced iris root bleeding
and anterior uveitis. Modern IOLs pose a significantly lower risk of inducing
UGH syndrome.
Treatment [I,D]:
yAnti-inflammatory treatment
yRemoval of silicone oil may be considered in eyes with IOP elevation
secondar y to silicon oil emulsification. However current data suggest
that removal of silicon oil is not ef fective in all cases and the risk of
re-detachment increases. Trans-scleral cyclophotocoagulation and aqueous
drainage devices seem to represent more ef fective options, although
the latter are associated with the risk of silicon oil escape into sub-
conjuctival space. Endoscopic cyclophotocoagulation in eyes requiring
silicon oil removal and antiglaucoma treatment seems to be ef fective
option. Conventional filtration surgery is associated with poor prognosis.
yRemoval of the intraocular lens may be needed in case of UGH syndrome
yGlaucoma surgery according to the specific condition
98
2.3.3 Secondary Open-Angle Glaucoma Caused By Extrabulbar Disease
2.3.3.1 Glaucoma caused by increased episcleral venous pressure
Etiology and pathogenic mechanism:

Episcleral, orbital or systemic diseases can cause the elevation of episcleral venous
pressure with subsequent reduction of trabecular outflow and IOP elevation. The
following disorders can be described:
yEpiscleral and orbital causes: chemical burn or radiation damage of the episcleral
veins, hemangioma in Sturge-Weber syndrome, Nevus of Ota, endocrine
orbitopathy, orbital (retrobulbar) tumor, pseudotumor, orbital phlebitis, orbital or
intracranial arteriovenous fistula
yNeurologic conditions: dural shunts, cavernous sinus thrombosis
yOther systemic causes: superior vena cava obstruction, jugular vein obstruction
(radical neck dissection), pulmonary venous obstruction
yIdiopathic forms
Symptoms and signs:

IOP elevation can be acute with eye irritation and pain. Visual acuity can be decreased.
Dilated, congested episcleral veins, chemosis, facial lymphedema, orbital bruit can be
present. Vascular bruits are characteristic signs of A/V fistulae120
Treatment [I,D]:
a) Treatment of the underlying disease
b) Topical and systemic IOP lowering medication
c) Glaucoma surgery
99
2.4 - PRIMARY ANGLE-CLOSURE

Scientific publications on angle-closure have suffered from the lack of a uniform definition
and specific diagnostic criteria. Only in recent years has there been recognition of the need
to standardize definitions of the various types.
Angle-closure is defined by the presence of iridotrabecular contact (ITC). This can be either
appositional or synechial. Either can be due to any one of a number of possible mechanisms.
Angle closure may result in raised IOP and cause structural changes in the eye. Primary
angle-closure (PAC) is defined as an occludable drainage angle and features indicating that
trabecular obstruction by the peripheral iris has occurred. The term glaucoma is added
if glaucomatous optic neuropathy is present: Primary angle-closure glaucoma (PACG).
The main reason to distinguish Primary angle-closure glaucoma from Primary open-angle
glaucoma is the initial therapeutic approach (i.e. iridotomy or iridectomy) and the possible
late complications (synechial closure of the chamber angle) or the complications resulting
when this type of glaucoma undergoes filtering surgery (uveal effusion, cilio-lenticular block
leading to malignant glaucoma)121,122.
The prevalence of primary angle closure glaucoma (PACG)

Ethnic background is one of the major factors determining susceptibility to primary
angle-closure (PAC). Population surveys show that PAC is more common among
people of Asian descent than those from Europe. Among people aged 40 years
and over, the prevalence of PAC ranges from 0.1% in Europeans123,124 through 1.4%
in East Asians123,124 and up to 5% in Greenland Inuit125. Of those over 40 years old in
European derived populations, 0.4% are estimated to have PACG. Three-quarters of
cases occur in female subjects. There are 1.60 million people in Europe and 581 000
people in the USA with PACG126.
Primary glaucoma cases should be examined and the anterior chamber angle shown to
be open on gonioscopy before PACG is excluded127.
Provocative Tests
In general provocative tests for angle-closure provide little additional information since even
when negative they may not rule out the potential for angle-closure. In addition they may
be hazardous, triggering an acute angle-closure attack even while the patient is monitored.
100
2.4.1 Primary Angle-Closure (PAC)
Angle-closure is defined by the presence of iridotrabecular contact (lTC). Gonioscopy remains

the standard technique for identifying ITC. Primary angle-closure (PAC) results from crowding
of the anterior segment, and as such, usually occurs in eyes with smaller than average anterior
segment dimensions. Pathological angle-closure is defined by the presence of ITC combined
with either elevated intraocular pressure (IOP) or peripheral anterior synechiae (PAS), or both.
The absence of ocular diseases which may induce the formation of PAS such as uveitis, iris
neovascularisation, trauma and surgery, defines primary angle-closure. Additionally, angle-
closure resulting from the action of forces at the level of the lens or behind the lens is usually
regarded as secondary (i.e. cataract, massive vitreous haemorrhage, and silicone oil or gas
retinal tamponade) as the successful management is aimed at the underlying lens or posterior
segment pathology. Angle-closure may impair aqueous outflow through simple obstruction of
the trabecular meshwork (TM), or by causing irreversible degeneration and damage of the TM.
2.4.1.1 Natural History of PAC
PAC becomes more likely as the separation between the iris and TM decreases128. The risk
of iridotrabecular contact in a “narrow” angle begins to increase once the iridotrabecular
angle is ≤ 20°129. With angles of 20° or less, signs of previous angle-closure, such as PAS or
iris pigment on the TM, should be carefully sought as signs of previous closure. Most angle-
closure occurs asymptomatically. Although symptoms of pain, redness, blurring of vision or
haloes may help identify people with significant angle-closure, the sensitivity and specificity
of symptoms for identifying angle-closure are very poor. The most commonly identified sign
which indicates that treatment is required is ITC. There is not a precise extent of gonioscopically
evident ITC which will dictate the indication to treatment for all cases.
An international group of experts reached a consensus that 2 quadrants or more of ITC is an
indication for prophylactic treatment130 [II,D].
Clearly, in established disease with high IOP, established PAS or glaucomatous optic
neuropathy, any potential for angle-closure should be considered and treated on individual
merits.
2.4.1.2 Staging of Primary Angle-closure123
a) Primary Angle-closure Suspect (PACS)

Two or more quadrants of iridotrabecular contact (lTC), normal IOP, no PAS, no
evidence of glaucomatous optic neuropathy (GON).
b) Primary Angle-closure (PAC)
Iridotrabecular contact resulting in PAS and/or raised IOP. No evidence of GON.
c) Primary Angle-closure Glaucoma (PACG)
Iridotrabecular contact causing GON; PAS and raised IOP may be absent at the time
of initial examination.
101
2.4.1.3 Ocular Damage in Angle-closure
Primary angle-closure (PAC) may cause ocular tissue damage in many ways. Corneal
endothelial cell loss occurs after symptomatic “acute” angle-closure. With very high
IOP values the iris may suffer ischaemic damage to musculature causing iris whirling
(distortion of radially orientated fibres) and/or a dilated, unresponsive pupil. The
lens epithelium may suffer focal necrosis causing anterior sub-capsular or capsular
opacity of the lens associated with focal epithelial infarct called “Glaukomflecken”.
The trabecular meshwork can be damaged by the formation of PAS, or as the result of
long- standing appositional closure. Optic neuropathy in angle-closure may manifest
in at least 2 ways. After an “acute” symptomatic episode, the disc may become pale
but flat, suggesting an anterior ischaemic optic neuropathy. Typical glaucomatous
optic neuropathy manifests in with an excavated surface and a pattern of visual field
loss indistinguishable from open-angle glaucoma. Angle-closure accounts for 50%
of all glaucoma blindness worldwide, and is probably the most visually destructive
form of glaucoma.
2.4.1.4 Outcome following treatment
In asymptomatic (“chronic”) angle-closure, a high presenting pressure (>35 mmHg),

more than 6 clock hours of peripheral anterior synechiae and/or established
glaucomatous optic neuropathy are signs that a case of angle-closure will not
respond fully to a laser iridotomy 131, and that a trabeculectomy may be needed to
control pressure” [II,D].
2.4.1.5 Mechanisms of angle-closure
It is important to identify secondary causes of narrow or closed-angles, such as

phakomorphic, uveitic and neovascular cases, as the management of these cases
is initially directed at controlling the underlying disease. In isometropic eyes it is
helpful to compare axial anterior chamber depths of the two eyes. Asymmetry of >
0.2 mm (3 standard deviations) is suggestive of a secondary pathological process.
A-mode or ultrasound biomicroscopy may be helpful in measuring axial dimensions
(Iength, AC depth and lens thickness) and defining anatomical relationships. In primary
angle-closure these will be the same in each eye. Mechanisms responsible for angle-
closure are described in terms of anatomical location of obstruction to aqueous flow,
successively, at the pupil, the iris and ciliary body, the lens and behind the lens. This
is also order of decreasing frequency of each mechanism. Two mechanisms may
co-exist, especially levels I and II (i.e. pupil and iris/ciliary body). Often, one mechanism
predominates.
I. Pupillary block mechanism

Pupillary block is the predominant mechanism in around 75% of cases of primary
angle-closure. Pupillary block is an exaggeration of a physiological phenomenon
in which the flow of aqueous from the posterior chamber through the pupil to the
102
anterior chamber is impeded causing the pressure in the posterior chamber to

become higher than the pressure in the anterior chamber. As a result, the peripheral
iris bows forward and comes into contact with the trabecular meshwork and/or
peripheral cornea.
In a minority of cases, this becomes a self-perpetuating cycle with obstruction of
trabecular outflow leading to a rise in IOP up to 50-80 mmHg. When total trabecular
obstruction occurs rapidly (within a few hours), it causes the symptoms and signs
of acute angle-closure (AAC).
The increased resistance to trans-pupillary aqueous flow is believed to result from
co-activation of both sphincter and dilator muscles, causing the pupil margin to
grip the anterior surface of the lens. This may occur in response to physiological
stimuli, such as reading in poor light, or pharmacologically, such as with miotic
therapy and concomitant dilator muscle stimulation by phenylephrine (the
Mapstone provocation test)132. In most cases, the predisposition to pupil block is
created by a narrow anterior segment and the age-related increase of lens volume
(See Ch. 2.5.1 and 2.5.3).
The prevalence of PAC is higher in elderly people women and in some races
(especially East Asians). There is a weaker association with hypermetropia,
exfoliation syndrome, diabetes and retinitis pigmentosa.
II. Anomalies at the level of the iris and/or ciliary body (“plateau iris configuration”)
This group of anterior, non-pupil-block mechanisms are sometimes erroneously
referred to under the umbrella term “plateau iris”. They are the result of variations
in iris and ciliary body anatomy that brings the peripheral iris into contact with the
trabecular meshwork. These include a thicker iris, a more anterior iris insertion and
a more anterior ciliary body position. These anatomical factors predict failure of a
laser iridotomy to open an appositionally closed angle133.
Anteriorly positioned ciliary processes cause “typical” plateau iris configuration134.
Plateau iris “syndrome” should be differentiated from plateau iris configuration.
The “configuration” refers to a situation in which the iris plane is flat and the
anterior chamber is not shallow axially. In most cases, the angle-closure glaucoma
associated with the plateau iris configuration is cured by a peripheral iridectomy.
“Plateau iris syndrome” refers to a post-laser condition in which a patent iridotomy
has removed the relative pupillary block, but gonioscopically confirmed angle closure
recurs without shallowing of the anterior chamber axially. Plateau iris syndrome is
rare compared to the configuration, which itself is not common. It usually occurs
in a younger age group than pupillary-block angle-closure. The treatment is laser
iridoplasty or the long-term use of pilocarpine postoperatively as long as it is needed
[II,D]. This syndrome must be considered in the differential diagnosis when the
intraocular pressure rises unexpectedly following an adequate peripheral iridectomy
procedure for angle-closure glaucoma135.
Ideally, treatment should be instituted before synechial closure of the angle occurs [II,D]
III. Anomalies at the Level of the Lens

The most widely recognised risk factor for primary angle-closure is a shallow anterior
chamber. The anterior surface of the lens marks the depth of the anterior chamber,
and as such, PAC patients typically have a thicker, more anteriorly positioned lens
103
than people with wide open angles. Nuclear sclerotic cataract is a frequent finding
in primary angle-closure. If a separate pathological or iatrogenic process causes
the lens to suddenly increase in thickness (e.g. “classic” diabetic or post-traumatic
cataract), become more anteriorly positioned (retinal gas or oil tamponade) or
subluxate (Marfan syndrome or trauma), this may cause secondary angle-closure (See
Ch. 2.5.1 and 2.5.3).
IV. Anomalies posterior to the Lens (Aqueous misdirection syndrome)

In rare cases, aqueous misdirection can complicate the management of primary
angle-closure. This may occur following trabeculectomy, lens extraction,
laser iridotomy and other surgical procedures. Forward movement of the lens
iris diaphragm causes secondary angle-closure resulting in IOP elevation.
These cases, typically have very small eyes (axial length <21 mm) and higher
hypermetropic refraction (> +6D). It is believed that the ciliary processes come into
contact with the lens equator, and/or a firm zonule/posterior capsule diaphragm,
causing misdirection of aqueous into the vitreous 135, 136. As a consequence, the
lens/iris diaphragm is pushed forward and occludes the anterior chamber angle.
After iridotomy or iridectomy, the use of miotics raises the IOP, whereas the
use of cycloplegics reduces the IOP. This ‘inverse’ or ‘paradoxical’ reaction to
parasympathomimetics should be tested only after iridotomy has been performed.
Ultrasound biomicroscopy can demonstrate abnormal posterior chamber anatomy
in these rare cases (See Ch. 2.5.3).
Asymmetry of anterior chamber depth is a cardinal sign of secondary (types III and
IV) angle-closure.
Systemic drugs and angle-closure

Systemic drugs which may induce angle-closure in pre-disposed individuals are:
nebulised bronchodilators (ipratropium bromide and/or salbutamol), selective
serotonin re-uptake inhibitors (SSRI’s), tricyclic antidepressants, proprietary cold and
flu medications, muscle relaxants, anti-epileptics (topiramate) and other agents with
a parasympatholytic and sympathomimetic action137.
2.4.1.6 Demographic risk factors for Primary Angle-Closure135,138
% Older age
% Female
% Asian and Eskimoan Race
Family history if primary angle-closure: family screening is vital in these families as robust
evidence now exists for significant increased risk of angle closure in family members
of an affected patient: first degree relatives may have a 1 in 4 risk of a PAC disease
requiring treatment139.
104
2.4.1.7 Descriptions of subtypes:
Primary angle-closure has previously been divided into 5 clinical subtypes according to
mode of presentation. There is debate on whether this approach to classification is useful in
determining the prognosis or optimal management.
% Primary Angle-Closure Suspect (PACS)

% Acute Angle-Closure (AAC)
% Intermittent Angle-Closure (IAC)
% Chronic Angle-Closure Glaucoma (CACG)
% Status Post-Acute Angle-closure Attack
2.4.1.7.1 Primary Angle-Closure Suspect (PACS) or “occludable” angle
Etiology and pathomechanism:

Pupillary block or plateau iris configuration; each component plays different roles in different
eyes (See Ch. 2.4.1.5).
Features:
Signs:
% Two or more quadrants of iridotrabecular contact (lTC)
% Normal IOP
% No peripheral anterior synechia (PAS)
% No evidence of glaucomatous optic neuropathy (GON)
% No glaucomatous visual field defect
The fellow eye of a documented non-secondary angle-closure is considered capable of
occlusion.
Treatment:
PACS or “occludable angle” is a clinical assessment. Whether to treat or not is the
responsibility of the ophthalmologist. There is not a precise extent of gonioscopically
evident ITC which will dictate the indication to treatment for all cases.
If a PAC suspect has narrow angle with two or more quadrants of ITC but no
synechial angle closure, the treatment to offer the patient is laser peripheral iridotomy
(LPI) followed by argon laser peripheral iridoplasty (ALPI) in cases with plateau iris
configuration [II,D].
The same applies to fellow eyes of primary angle-closure [I,C]. All cases must be
assessed individually [I,D]. In general, the risks of treatment are to be balanced against
the perceived risk of angle-closure.
2.4.1.7.2 Acute Angle-Closure (AAC) with pupillary block mechanism
Etiology:
Circumferential iris apposition to the trabecular meshwork with rapid and excessive increase
in IOP that does not resolve spontaneously.
105
Pathomechanism:
See Ch. 2.4.1.5
Features:
Signs:
% IOP >21 mmHg, often to 50-80 mmHg.
% Decreased visual acuity
% Corneal oedema, initially mostly epithelial oedema. Shallow or flat peripheral
anterior chamber
% Peripheral iris pushed forward and in contact with Schwalbe’s line. Gonioscopy:
iridotrabecular contact 360°
% Pupil mid-dilated and reduced or no reactivity
% Venous congestion and ciliary injection
% Fundus: disc oedema, with venous congestion and splinter haemorrhages, or
the disc may be normal or show glaucomatous excavation
% Bradycardia or arrhythmia
% Gonioscopy clues from the other eye
Symptoms:
% Blurred vision, “halos” around lights
% Pain
% Frontal headache of variable degree on the side of the affected eye
% Nausea and vomiting, occasionally
% Palpitations, abdominal cramps, occasionally
Treatment options:
See also flowchart FC VII-VIII
A. Medical treatment
B. Laser peripheral iridotomy (LPI)
C. Argon Laser Peripheral Iridoplasty (ALPI)
D. Lens Extraction
E. Trabeculectomy
F. Anterior Chamber Paracentesis
G. Goniosynechialysis (GSL)
Iridotomy or iridectomy together with medical treatment is the preferred definitive treatment
of acute angle-closure glaucoma with a pupillary block component [I,D]
A: Medical Treatment [I,D]

Medical treatment serves to lower IOP, to relieve the symptoms and signs so that laser
iridotomy or iridectomy is possible
Medical therapy aims for
1. withdrawal of aqueous from vitreous body and posterior chamber by
hyperosmotics
2. pupillary constriction to open the chamber angle
3. reduction of aqueous production reduction of inflammation.
106
All the above steps of medical therapy should be implemented concurrently [I,D]
Consider contraindications to each of the medications to be used
yReduction of aqueous production

o acetazolamide 10 mg/Kg intravenously or orally. Topical carbonic anhydrase
inhibitors (CAls) are not potent enough to break the pupillary block
o topical alpha-2 agonists
o topical beta-blockers
yDehydration of vitreous body
Hyperosmotics are the effective agents but carry significant systemic risk in some
patients: patients must be evaluated for heart or kidney disease because hyperosmotics
increase blood volume which increases the load in the heart [IID]. Glycerol may alter
glucose blood levels and should not be given to diabetics (FC VII) [I,D]
- glycerol 1.0 - 1.5 g/Kg orally
- mannitol 1.0 - 1.5 g/Kg intravenously
yPupillary constriction [I,D]

o pilocarpine 1% or 2% or aceclidine 2% twice or three times within 1 hour
Note: while the sphincter is ischaemic and the pupil non-reactive to light for sphincter
paresis, multiple applications of topical parasympathomimetics is not helpful, will not
cause pupillary constriction and may cause forward rotation of the ciliary muscle,
thereby increasing the pupillary block. Since miotics in large doses can cause
systemic side effects due to trans-nasal absorption leading to abdominal spasms and
sweating, intensive topical parasympathomimetics are no longer indicated to treat
this condition.Miotics are likely to constrict the pupil only after IOP has been lowered.
o dapiprazole 0.5%
o Alpha-1 blockers relax the dilator muscle. They do not reduce pupil size when
the sphincter-muscle is paretic.
yReduction of inflammation
Topical steroid every 5 minutes for three times, then 4-6 times daily, depending
on duration of raised IOP and severity of inflammation.
B: Surgical Treatment
yNeodymium YAG laser iridotomy
Laser iridotomy should be attempted if the cornea is sufficiently clear [I,C]. Argon
laser iridotomy is rarely performed nowadays but thermal laser pre-treatment
(e.g,. argon) of dark irides reduces total YAG energy required127 [II,B]
ySurgical iridectomy
1) Transcorneal approach.
o Advantages:
- No conjunctival scarring
- A water-tight self-sealing incision is possible
107
o Disadvantages:
- Technically more difficult in dilated fixed pupil and flat anterior
chamber
- More traction an iris with increased risk of haemorrhage
2) Corneoscleral approach
o Advantages:
- Iridectomy can be basal
o Disadvantages:
- Conjunctival wound may lead to scarring compromising the
outcome of a filtering procedure which may become necessary at
a later stage insufficient wound closure and aqueous misdirection
may occur in rare cases
3) General advantages of surgical iridectomy:

- It can be performed even when the cornea is cloudy
- It allows deepening of the anterior chamber, breaking freshly
formed PAS
4) General disadvantages of surgical iridectomy:

- All the potential risks of any intraocular procedure in an eye with
angle closure
C: Argon Laser Peripheral Iridoplasty (ALPI)

There is now some evidence from randomised controlled trials that ALPI can break
an attack of acute angle closure as or more swiftly than medical therapy140. Many
glaucoma specialists now routinely use ALPI if topical treatment + acetazolamide have
not broken an attack within an hour, prior to considering hyper-osmotics. ALPI is also
a useful procedure to eliminate appositional angle closure resulting from mechanisms
other than pupillary block (i.e: plateau iris configuration)141.
Diode Laser Peripheral Iridoplasty has greater penetration of an oedematous cornea but
has been less extensively studied.
Anterior chamber paracentesis is being evaluated to break the attack in cases that are
refractory to medical management142.
D: Lens extraction See FC VII

Clinical reports of phacoemulsification with posterior chamber intraocular lens
implantation in the treatment of acute, chronic, and secondary angle-closure +/-
glaucoma describe very favourable results. The appropriate role for lensectomy
in the management of primary angle closure, however, still remains unproven.
The first case-series study showed that cataract extraction was associated with
a good reduction in IOP and a reduction in the number of medications required
to control IOP143.
A few prospective case series or randomized clinical trials have been performed143-146
or are ongoing147 to determine the value and comparative risks and efficacy of lens
surgery, both clear lens extraction and cataract surgery, versus medical therapy,
laser peripheral iridotomy, laser iridoplasty, and filtration procedures for the treat-
108
ment of acute and chronic primary angle closure and for the prevention of chronic
angle-closure glaucoma, both after and instead of laser peripheral iridotomy.
Cataract surgery in PACG is generally more challenging and prone to complications
than in normal eyes or eyes with POAG because of the shallow AC, larger lens,
corneal oedema, poorly dilated or miotic pupil, extensive posterior synechiae, lower
endothelial cell count, weaker zonules, especially after an acute angle closure attack.
In an eye with a clear lens: laser PI first. If the angle does not open and IOP not
well controlled with unquestionable glaucomatous damage, consider to proceed with
phacoemulsification and IOL implantation [I,D].
E: Trabeculectomy
Trabeculectomy in chronic PACG is also associated with higher risk of postoperative
anterior chamber shallowing, malignant glaucoma, and a significant rate of cataract
formation compared to POAG137. Even when filtration surgery has successfully
reduced the IOP, the ailing trabecular meshwork does not regain its function, and
so the disease is not cured.
Combined lens extraction and trabeculectomy

In a study in CACG eyes with coexisting cataract, combined phacotrabeculectomy
resulted in significantly more surgical complications than phacoemulsification alone.
Visual acuity or disease progression did not differ between the 2 treatment groups148.
F: Anterior Chamber Paracentesis139, 142

yRapidly lowers IOP in APAC
yInstantaneous relief of symptoms
yPrevention of further optic nerve and trabecular meshwork damage
secondary to the acutely elevated IOP
yThe IOP-lowering benefit may decrease by 1 hour after the procedure
y Anti-glaucoma medications are necessary to maintain IOP control.
Paracentesis will not directly break the pupillary block but can allow the cornea to clear
permitting to perform LPI
Possible complications include

yExcessive shallowing of the anterior chamber
yPuncture of iris, lens
yChoroidal effusion
yHaemorrhage due to the sudden decompression
G: Goniosynechialysis138
Often performed with other procedures such as lens extraction, to detach synechia from
the angle, in eyes with minimal to moderate optic nerve damage.
The procedure may be complicated by:
yhyphema
yfibrinous inflammation and
yrecurrent synechial closure of the angle
109
2.4.1.7.3 Acute Angle-Closure (AAC) with plateau iris configuration (See FC VII)
In plateau iris configuration the iris plane is flat and the anterior chamber is not shallow axially.
(See above under Staging of Primary Angle-closure).
Medical treatment [II,D]:

yPupillary constriction to pull the peripheral iris centripetally
yIn plateau iris configuration, a modest pupillary constriction may prevent further
angle- closure
- pilocarpine 1%, aceclidine 2%, carbachol 0.75%
- dapiprazole 0.5%
Surgical treatment [I,D]:

yIridotomy is essential to confirm the diagnosis because it eliminates any pupillary
block component
yArgon Laser Peripheral Iridoplasty (ALPI) stretches the iris and widens the chamber
angle149.
“Plateau iris syndrome” refers to a post-laser iridotomy condition in which a patent iridotomy
has removed the relative pupillary block, but gonioscopically confirmed angle closure recurs
without central shallowing of the anterior chamber. Isolated plateau iris syndrome is rare
compared to the plateau configuration, which itself is not common. It usually occurs in a
younger age group than pupillary-block angle-closure. The treatment is laser iridoplasty or
the long-term use of pilocarpine postoperatively [II,D]. This condition must be considered
in the differential diagnosis when the intraocular pressure rises unexpectedly following an
adequate peripheral iridectomy procedure for angle-closure glaucoma135.
2.4.1.7.4 Intermittent Angle-Closure (lAC)
Etiology:
Similar but milder clinical manifestations than AAC, it resolves spontaneously.
Pathomechanism:
See above Ch. 2.4.1.5
Features:
Signs:
% May vary according to amount of iridotrabecular contact of chamber angle and
mimic acute angle-closure in a mild form
% When not on miotics, pupil is round and reactive
% The optic disc rim may show atrophy with an afferent pupillary defect
Symptoms:
% Mild, intermittent symptoms of acute angle-closure type
110
Treatment:
Pupillary constriction, iridotomy, iridoplasty or lens extraction are to be considered according
to the main mechanism determining angle occlusion [II,D]
FC VII - Management of Acute Primary Angle

Closure Attack
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2.4.1.7.5 Chronic Angle-Closure Glaucoma (CACG) (See FC VIII)
Etiology:
Permanent synechial closure of any extent of the chamber angle as confirmed by indentation
gonioscopy.
Pathomechanism:
See Ch. 2.4.1.5
Features:
Signs:
% Peripheral anterior synechiae of any degree at gonioscopy
% IOP elevated to a variable degree depending on the extent of iridotrabecular
contact, above 21 mmHg
% Visual acuity according to functional status (may be normal)
% Damage of optic nerve head compatible with glaucoma
% Visual field defects “typical” of glaucoma may be present
% Superimposed intermittent or acute iridotrabecular contact possible
Symptoms:
% Visual disturbances according to functional states.
% Usually no pain; sometimes discomfort
% Transient “halos” when intermittent closure of the total circumference causes
acute IOP elevations
Treatment:
Medical treatment alone is contraindicated as all patients require relief of pupil block by iridotomy,
iridectomy or lens extraction [I,D]. If the synechial closure is less than half the circumference,
iridectomy/iridotomy may be sufficient.
Since complications of iridotomy are uncommon, its use as the initial procedure is justified in
practically every case [I,D].
Argon laser trabeculoplasty is contraindicated as it may increase synechial angle-closure [I,D].
Lens removal may be considered at all stages and can lead to relief of pupil block and sufficient
IOP control [II,D].
If IOP cannot be controlled medically after breaking pupil block (with or without lens extraction),
a filtering procedure is indicated [II,D].
These eyes are more frequently prone to develop posterior aqueous misdirection and the
necessary precautions must be taken when considering surgery.
2.4.1.7.6 Status Post-Acute Angle-closure Attack
Etiology:
Previous episode of acute angle-closure attack
Pathomechanism:
See Ch. 2.4.1.5
112
Features:
Signs:
% Patchy iris atrophy Iris torsion/spiralling posterior synechiae
% Pupil either poorly reactive or non-reactive
% “Glaukomflecken” of the anterior lens surface
% Peripheral anterior synechiae on gonioscopy
% Endothelial cell count can be decreased
Therapy:
Management according to angle, lens, IOP and disc/visual field. In case of cataract surgery,
non dilatable pupil, low endothelial cell count and loose zonules are of concern.
FC VIII - Management of Chronic Angle Closure
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113
2.5 - SECONDARY ANGLE-CLOSURE

There are many different causes of secondary angle-closure and the clinical signs vary
according to the underlying condition. For example in secondary acute angle-closure,
the chamber angle is closed by iridotrabecular contact that can be reversed, whereas in
chronic secondary angle-closure, the angle-closure is irreversible due to peripheral anterior
synechiae.
A complete discussion of these topics is outside the scope of this text.
2.5.1 Secondary Angle-Closure With Pupillary Block
Etiology:
The following is a limited list of other etiologies for relative or absolute pupillary block:
% Enlarged, swollen lens (cataract, traumatic cataract)
% Anterior lens dislocation (trauma, zonular laxity; Weil-Marchesani’s syndrome,
Marfans’s syndrome etc.)
% Posterior synechiae, seclusion or occlusion of the pupil
% Protruding vitreous face or intravitreal silicone oil in aphakia
% Microspherophakia
% Miotic-induced pupillary block (also the lens moves forward)
% IOL-induced pupillary block; anterior chamber IOL, phakic intraocular lens
(PIOL), anteriorly dislocated posterior chamber intraocular lens (PC-IOL)150
Pathomechanism:
Pupillary block pushes the iris forward to occlude the angle. In iritis or iridocyclitis, the
development of posterior synechiae may lead to absolute pupillary block with consequent
forward bowing of the iris or “iris bombé”. Acute secondary angle-closure glaucoma may
result.
Features:
y IOP>21 mmHg
y Disc features compatible with glaucoma
Treatment:
Several steps may be considered, according to the clinical picture of causative
mechanisms [II,D]
y Topical and systemic IOP lowering medication
y Nd:YAG laser iridotomy
y Peripheral surgical iridectomy
y Lens extraction, vitrectomy
y Discontinuing miotics in miotic-induced pupillary block
y Pupillary dilation
y Nd:YAG laser synechiolysis of posterior synechiae
114
2.5.2 Secondary Angle-Closure With Anterior “Pulling” Mechanism Without

Pupillary Block
Pathomechanism:
The trabecular meshwork is obstructed by iris tissue or a membrane. The iris and/or a
membrane are progressively pulled forward to occlude the angle.
Features:
yIOP>21 mmHg
yDisc features compatible with glaucoma
2.5.2.1 Neovascular glaucoma
The iridotrabecular fibrovascular membrane is induced by ocular microvascular disease with

retinal ischemia; initially the neovascular membrane covers the angle, causing a secondary
form of open angle glaucoma (See Ch 2.3 Secondary Open Angle Glaucoma)
Treatment [II,D]:
a) Topical atropine or equivalent
b) Topical steroid initially
c) Topical and systemic IOP lowering medication as needed
d) Retinal ablation with laser or cryotherapy
e) Cyclodestruction
f) Filtering procedure with antimetabolites
g) Aqueous drainage devices
h) Miotics are contraindicated
The intravitreal injection of anti-VEGF molecules has shown benefit for this indication [II,C]
and is in widespread use.
2.5.2.2 Iridocorneal endothelial syndrome
Iridocorneal Endothelial (ICE) Syndrome, with progressive endothelial membrane formation

and progressive iridotrabecular adhesion.
Peripheral anterior synechiae, due to prolonged primary angle-closure; this is theoretically a
primary angle-closure.
Treatment [II,D]:
a) Topical and systemic IOP lowering medications as needed
b) Filtering procedure, with antimetabolite according to risk factors
c) Aqueous drainage device
115
2.5.2.3 Posterior polymorphous dystrophy
Treatment [II,D]:
a) Topical and systemic IOP lowering medication as needed
b) Filtering procedure, with antimetabolite according to risk factors
2.5.2.4 Epithelial and fibrous ingrowth after anterior segment surgery or penetrating
trauma
Epithelial and fibrous ingrowth after anterior segment surgery or penetrating trauma
Inflammatory membrane.
Treatment [II,D]:
b) Excision, destruction of the immigrated tissue
c) Filtering procedure, with antimetabolite according to risk factors
d) Aqueous drainage device
e) Cyclodestruction
2.5.2.5 Inflammatory membrane
Treatment [II,D]:
a) Anti-inflammatory medications and cycloplegics
b) Topical and systemic IOP lowering medication as needed
c) Filtering procedure with antimetabolite
e) Cyclodestruction
2.5.2.6 Peripheral anterior synechiae after ALT and endothelial membrane covering
the trabecular meshwork late after ALT
After argon laser trabeculoplasty (ALT), early and late peripheral anterior synechiae and
endothelial membrane covering the trabecular meshwork
Treatment [II,D]:
b) Filtering procedure
2.5.2.7 Aniridia
Treatment [II,D]:
b) Trabeculotomy
116
c) Filtering procedure with antimetabolites

e) Cyclodestruction
2.5.3 Secondary Angle-Closure With Posterior ‘Pushing’ Mechanism Without

Pupillary Block
2.5.3.1 Aqueous misdirection (also known as cilio-lenticular block, ciliary block or

malignant glaucoma)
Etiology:
Angle-closure is caused by the ciliary body and iris rotating forward. Aqueous
misdirection, or malignant glaucoma, is a rare type of secondary angle-closure
glaucoma most commonly encountered after filtering surgery. The syndrome, also
known as ciliary block glaucoma, can occur spontaneously or following any type of
intraocular surgery.
Pathomechanism:
% The lens may be proportionally abnormally large or swollen, “phacomorphic glaucoma”
% Aqueous humour accumulates in the vitreous body (posterior aqueous humour
misdirection) or behind and around the crystalline lens (perilenticular misdirection)
or behind the iridocapsular diaphragm or posterior chamber intraocular lens (PCL)
after extracapsular cataract surgery, with or without PCL implantation, “retrocapsular
misdirection”
% Frequently precipitated by ocular surgery and flat anterior chamber
% Predisposition may be similar in both eyes particularly in small eyes
Treatment:
Medical treatment
a) Parasympatholytics (atropine, cyclopentolate) both initially and for long-term
pupillary dilation and cycloplegia [I,C]
b) Aqueous production suppressants given orally and/or topically [I,D]
c) Hyperosmotics (Ch. 3.3.1.3) [I,D]
Miotics are contraindicated!
Surgical treatment
a) A patent iridotomy must be present or, if not present, iridotomy should be
performed [I,D]
b) YAG laser vitreolysis/capsulotomy, especially in aphakia, pseudophakia [II,C]
c) Anterior vitrectomy, especially in aphakia, pseudophakia [II,C]
d) Cyclo diode laser
e) In selected cases lens extraction [II,D]
117
2.5.3.2 Iris and ciliary body cysts, intraocular tumors
Treatment:
a) Tumour irradiation or excision
b) Filtering surgery
c) Cyclodestruction
2.5.3.3 Silicon oil or other tamponading fluids or gas implanted in the vitreous cavity138
Treatment:
a) Topical/systemic IOP lowering medications as needed
b) Silicon oil or gas aspiration
c) Filtering surgery
d) Drainage device
e) Cyclodestruction
2.5.3.4 Uveal effusion151,152
It is due to:
y Inflammation as in scleritis, uveitis, HIV infection
y Increased choroidal venous pressure as in nanophthalmos, scleral buckling,
panretinal photocoagulation, central retinal vein occlusion, arterio-venous
communication
y Tumor
Treatment:
a) Anti-inflammatory medication (for 1)
b) Topical and systemic IOP lowering medication as needed (for 1,2 and 3)
c) Relaxation of scleral buckling; vitrectomy, sclerectomy in nanophthalmus (for Tumor
excision or irradiation (for 3)
d) Cyclodestruction
2.5.3.5 Retinopathy of prematurity (stage V)
Features:
Signs and Symptoms:
y Variable discomfort, pain, redness, corneal oedema IOP ≥ 21 mmHg
y Axially shallow anterior chamber
Treatment:
a) Topical and systemic IOP lowering medications
b) Cyclodestruction
c) Filtering procedure with or without antimetabolite
d) Drainage devices
118
2.5.3.6 Congenital anomalies that can be associated with secondary glaucoma
These conditions are extremely variable in pathogenesis, clinical presentation and required
management; an extensive discussion is outside the scope of this chapter.
Etiology:
Familial iris hypoplasia, anomalous superficial iris vessels, aniridia, Sturge-Weber
syndrome, neurofibromatosis, Marfan’s syndrome, Pierre Robin syndrome, homocystinuria,
goniodysgenesis, Lowe’s syndrome, microcornea, microspherophakia, rubella, broad thumb
syndrome, persistent hyperplastic primary vitreous.
Pathomechanism:
Angle-closure is caused by pushing forward the ciliary body and iris.
Increase of volume of the posterior segment of the eye.
Features:
Signs and Symptoms:
y IOP> 21 mmHg
y Pain, redness, corneal oedema
y Axially shallow anterior chamber
y Laser iridotomy and surgical iridectomy are not effective
Some differential diagnoses:

Acute IOP elevation with corneal oedema but open-angle may result from Posner
Schlossman syndrome (iridocyclitic crisis), or from endothelitis/trabeculitis as in disciform
herpetic keratitis.
Neovascular glaucoma may be associated with an open or closed-angle and may mimic
some signs and the symptoms of acute angle-closure.
Some differential diagnoses:

Acute IOP elevation with corneal oedema but open-angle may result from Posner
Schlossman syndrome (iridocyclitic crisis), or from endothelitis/trabeculitis as in disciform
herpetic keratitis.
Neovascular glaucoma may be associated with an open or closed-angle and may mimic
some signs and the symptoms of acute angle-closure.
Treatment:
Treatment to be adapted to the primary anomaly, the mechanism of IOP elevation and
the quality of life of the patient.
119
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intravitreal injection of triamcinolone acetonide. Bull Soc Belge Ophtalmol 2004(292):45-51.
116. Jones R, 3rd, Rhee DJ. Corticosteroid-induced ocular hypertension and glaucoma: a brief
review and update of the literature. Curr Opin Ophthalmol 2006;17(2):163-7.
117. Mangouritsas G, Mourtzoukos S, Portaliou DM, et al. Glaucoma associated with the
management of rhegmatogenous retinal detachment. Clin Ophthalmol 2013;7:727-34.
118. Lalezary M, Kim SJ, Jiramongkolchai K, et al. Long-term trends in intraocular pressure
after pars plana vitrectomy. Retina 2011;31(4):679-85.
119. Ichhpujani P, Jindal A, Jay Katz L. Silicone oil induced glaucoma: a review. Graefes Arch
Clin Exp Ophthalmol 2009;247(12):1585-93.
120. Nassr MA, Morris CL, Netland PA, Karcioglu ZA. Intraocular pressure change in orbital
disease. Surv Ophthalmol 2009;54(5):519-44.
121. Liebmann JMR, R. Complications of glaucoma surgery. In: Mosby SL, ed. Ritch R, Shields
MB, Krupin T The Glaucomas1986.
122. Simmons RJM, F.A. Malignant Glaucoma. In: Mosby SL, ed. Ritch, R Shields, MB Krupin,
T: The Glaucomas 1996.
123. Foster PJ, Buhrmann R, Quigley HA, Johnson GJ. The definition and classification of
glaucoma in prevalence surveys. Br J Ophthalmol 2002;86(2):238-42.
124. Foster PJ, Johnson GJ. Glaucoma in China: how big is the problem? Br J Ophthalmol
2001;85(11):1277-82.
125. Congdon N, Wang F, Tielsch JM. Issues in the epidemiology and population-based
screening of primary angle-closure glaucoma. Surv Ophthalmol 1992;36(6):411-23.
126. Day AC, Baio G, Gazzard G, et al. The prevalence of primary angle closure
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glaucoma in European derived populations: a systematic review. Br J Ophthalmol

2012;96(9):1162-7.
127. De Silva DJ, Gazzard G, Foster P. Laser iridotomy in dark irides. Br J Ophthalmol
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128. Foster PJ, Aung T, Nolan WP, et al. Defining “occludable” angles in population surveys:
drainage angle width, peripheral anterior synechiae, and glaucomatous optic neuropathy in
East Asian people. Br J Ophthalmol 2004;88(4):486-90.
129. Becker B, Shaffer RN. Diagnosis and therapy of the glaucomas. St. Louis: C. V. Mosby
Co., 1961; 360 p.
130. Friedman DSW, R. N. Consensus on Angle-closure and Angle-closure Glaucoma. AIGS/
WGA Consensus Series 2008.
131. Salmon JF. Long-Term Intraocular Pressure Control After Nd-YAG Laser Iridotomy in
Chronic Angle-Closure Glaucoma. J Glaucoma 1993;2(4):291-6.
132. Mapstone R. Provocative tests in closed-angle glaucoma. Br J Ophthalmol
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133. He M, Friedman DS, Ge J, et al. Laser peripheral iridotomy in eyes with narrow drainage
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134. Ritch R. Plateau Iris Is Caused by Abnormally Positioned Ciliary Processes. J Glaucoma
1992;1(1):23-6.
135. Wand M, Grant WM, Simmons RJ, Hutchinson BT. Plateau iris syndrome. Trans Sect
Ophthalmol Am Acad Ophthalmol Otolaryngol 1977;83(1):122-30.
136. Lowe RF. Primary Angle-Closure Glaucoma. Family Histories and Anterior Chamber
Depths. Br J Ophthalmol 1964;48:191-5.
137. Lachkar Y, Bouassida W. Drug-induced acute angle closure glaucoma. Curr Opin
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138. Tanihara H, Nishiwaki K, Nagata M. Surgical results and complications of goniosynechialysis.
139. Lam DS, Chua JK, Tham CC, Lai JS. Efficacy and safety of immediate anterior chamber
paracentesis in the treatment of acute primary angle-closure glaucoma: a pilot study.
140. Lai JS, Tham CC, Chua JK, et al. To compare argon laser peripheral iridoplasty (ALPI)
against systemic medications in treatment of acute primary angle-closure: mid-term results.
Eye (Lond) 2006;20(3):309-14.
141. Ritch R, Tham CC, Lam DS. Argon laser peripheral iridoplasty (ALPI): an update. Surv
Ophthalmol 2007;52(3):279-88.
142. Arnavielle S, Creuzot-Garcher C, Bron AM. Anterior chamber paracentesis in patients
with acute elevation of intraocular pressure. Graefes Arch Clin Exp Ophthalmol
2007;245(3):345-50.
143. Greve EL. Primary angle closure glaucoma: extracapsular cataract extraction or filtering
procedure? Int Ophthalmol 1988;12(3):157-62.
144. Tarongoy P, Ho CL, Walton DS. Angle-closure glaucoma: the role of the lens in the
pathogenesis, prevention, and treatment. Surv Ophthalmol 2009;54(2):211-25.
145. Lai JS, Tham CC, Chan JC. The clinical outcomes of cataract extraction by
phacoemulsification in eyes with primary angle-closure glaucoma (PACG) and co-existing
cataract: a prospective case series. J Glaucoma 2006;15(1):47-52.
146. Husain R, Gazzard G, Aung T, et al. Initial management of acute primary angle closure:
126
a randomized trial comparing phacoemulsification with laser peripheral iridotomy.

Ophthalmology 2012;119(11):2274-81.
147. Azuara-Blanco A, Burr JM, Cochran C, et al. The effectiveness of early lens extraction with
intraocular lens implantation for the treatment of primary angle-closure glaucoma (EAGLE):
study protocol for a randomized controlled trial. Trials 2011;12:133.
148. Tham CC, Kwong YY, Leung DY, et al. Phacoemulsification vs phacotrabeculectomy in
chronic angle-closure glaucoma with cataract: complications [corrected]. Arch Ophthalmol
2010;128(3):303-11.
149. Ritch R, Tham CC, Lam DS. Long-term success of argon laser peripheral iridoplasty in the
management of plateau iris syndrome. Ophthalmology 2004;111(1):104-8.
150. Traverso CE, Tomey KF, Gandolfo E. The glaucomas in pseudophakia. Curr Opin
Ophthalmol 1996;7(2):65-71.
151. Nash RW, Lindquist TD. Bilateral angle-closure glaucoma associated with uveal effusion:
presenting sign of HIV infection. Surv Ophthalmol 1992;36(4):255-8.
152. Moorthy RS, Mermoud A, Baerveldt G, et al. Glaucoma associated with uveitis. Surv
Ophthalmol 1997;41(5):361-94.
127
128
CHAPTER 3
Treatment
Principles and Options
129
Treatment Principles and Options
130
Treatment
Principles and Options
3.1 - GENERAL PRINCIPLES OF GLAUCOMA TREATMENT
The purpose of this chapter is to give a summary overview and it is not meant to be
an all-inclusive text
Normal
vision
Severe
functional
impairment
C
Age at disease onset Death

Blindness
Figure 3.1. THE WHOM -TO -TREAT GRAPH The rate of ganglion cell loss and resulting functional decay
is very different among different glaucoma eyes. Quality of life is clearly reduced when visual field defects
become severe, cf. the severe functional impairment. Line A represents the effect of aging alone. In glaucoma
loss of visual function is often much more rapid. An older patient, diagnosed late in life, with a moderate rate
of progression (B) has a much lower risk of developing severe functional impairment than a younger patient
with the same amount of field loss at diagnosis and rate of progression (C). A very slow rate of progression
may be tolerated by the patient and treatment left unchanged (D), while a rapid rate of progression (E) needs
a considerably lower target pressure.
It needs to be remembered that it is the extent of binocular visual field or the field of the better eye that largely
determines the patient’s quality of life, while the rates of progression of each eye separately are needed to
determine treatment.
To assess the likely Rate of Progression (RoP) is an important part of patient management
and the measured rate is a very important factor that should determine target pressure and
treatment intensity (See Ch. Introduction) [I.D]. Many studies have found that progression
is usually linear1-4, but the goal of intensifying treatment is to decrease rate of progression.
131
Please observe that perimetric printouts of progression using the MD or VFI indices are
age-corrected, so that a normal eye would not show any age-related deterioration over
time.
The goal of glaucoma treatment is to maintain the patient’s visual function and related
quality of life, at a sustainable cost. The cost of treatment in terms of inconvenience
and side effects as well as financial implications for the individual and society
requires careful evaluation (See Ch. Introduction). Quality of life is closely linked
with visual function and, overall, patients with early to moderate glaucoma damage
have good visual function and modest reduction in quality of life, while quality of life
is considerably reduced if both eyes have advanced visual function loss.
Glaucoma is still a leading cause of blindness in Europe. A considerable percentage

of glaucoma patients become blind in both eyes or encounter serious field loss in
both eyes 5-7. Major risk factors for glaucoma blindness are the severity of the disease
at presentation and life expectancy 8,9. A 60-year-old patient with bilateral moderate
visual function damage at diagnosis has a greater risk of blindness than an 85-year-old
patient with a similar amount of damage. Similarly a young patient with mild bilateral
damage is at much larger risk of disability in his lifetime than an 80-year-old patient
with moderate unilateral disease Thus, treatment must be individualised to the needs
and rate of progression (RoP) of each patient (See Fig. 1 Ch. Introduction) [I,D]. The
risk of ever encountering loss of quality of life from glaucoma should determine target
pressure, intensity of treatment, and frequency of follow-up [I,D].
Thus, patients with severe functional loss or younger patients with manifest disease
should have more aggressive treatment and closer follow-up than patients with little or
no risk, e.g., very old patients with early field loss or unilateral disease [I,D]. Glaucoma
suspects, e.g., patients with elevated IOP and otherwise normal findings, have
even smaller risks.
In most patients with advanced glaucoma and reasonable life expectancy, aggressive
IOP lowering treatment might be recommended10,11 [I,D]. Very old patients with mild
loss, relatively low IOP levels and significant health problems, might prefer being
followed without treatment (See also Ch. Introduction) [II,D]. When treatment options
are discussed with a patient, his general health status and personal preferences must
be considered and respected. It is also important to ensure that patients are able to
comply and persist with therapy [I,D].
Disease progression rates (RoP) in POAG, the most common form of glaucoma differ
very much between patients, from rapid to very slow12-16. This makes it necessary to
determine the RoP in patients with manifest glaucoma (See Fig. 1 Ch. Introduction) [I,D].
Many patients with POAG/NTG show no or only small deterioration despite years
of follow-up 17,18, while rapid progression is common in others, e.g. in exfoliation
glaucoma18. Glaucoma patients may continue to show progression despite treatment,
even with IOP levels within the statistically normal range. Relying on tonometry alone
for glaucoma follow-up is, therefore, insufficient regardless of IOP level17,18.
Determining the rate of visual field progression is a new standard in glaucoma care.
The EGS recommends three visual field tests per year for the first two years after
132
diagnosis to make it possible to identify rapidly progressing patients [II,D]. After two
years of perimetric monitoring without progression being detected the frequency of
tests may be reduced [II,D].
Once the progression rate has been determined the target pressure is re-evaluated
and be based on the measured rate of progression and IOP values measured during
the follow-up time [II,D]. Risk factors are then less important than at diagnosis (See
Ch. 2.2).
Individualized glaucoma treatment aims at providing glaucoma management tailored

to the individual needs of the patient; patients with severe functional loss or younger
patients with manifest disease should have more aggressive treatment and closer
follow-up than patients with little or no risk, e.g., patients with ocular hypertension or
elderly patients with mild field loss and low IOP levels19-23 [I,D]. (See FC VI)
In most Western countries approximately half of patients with manifest glaucoma are
undiagnosed24-27, and glaucoma is often diagnosed late8. Improved case finding and possibly
screening of high risk groups are necessary to allow diagnosis at earlier disease stages.
Screening options for high risk groups should be evaluated. To discover and treat those at
risk of losing functionally significant vision is a more important goal for effective glaucoma
management than widespread treatment of patients with ocular hypertension.
Currently, the only approach proven to be efficient in preserving visual function is lowering
IOP28-31 (See Ch. Introduction and FC VI to XI) [I,A]. Other possible treatment areas have been
investigated, including ocular blood flow and neuroprotection. There are experimental as well
population based studies indicating that perfusion pressure may be relevant in glaucoma31-37
but very difficult to measure38 a specific glaucoma phenotype characterised by vascular
dysregulation has been described32,33. An increase of IOP will lead to a reduction of perfusion
pressure. Blood pressure levels may also be important in glaucoma17,36,37. However, there
is no conclusive evidence to support the idea that perfusion pressure can be increased by
manipulating blood pressure or ocular blood flow in glaucoma patients.
Neuroprotection can be defined as a “therapeutic approach” aiming to directly prevent,
hinder and, in some cases, reverse neuronal cell damage. Since glaucoma patients can
continue deteriorating in spite of an apparently well controlled IOP, the need for effective
non-IOP related treatments is widely acknowledged. Several compounds have been shown
to be neuroprotective in animal models of experimental glaucoma39-43.
So far, no compound has reached a sufficient level of evidence to be considered as a
neuroprotectant in humans. A large long-term randomized trial using a neuroprotective
agent, memantine, was analysed several years ago, but with negative results. A more
recent study claiming that topical brimonidine might haven neuro-protective properties
in glaucoma patients, has been questioned in a systematic review on neuroprotection in
glaucoma44,45.
In most western countries, approximately half of patients with manifest glaucoma

are undiagnosed24-27.
133
3.2 - TARGET IOP AND QUALITY OF LIFE
3.2.1 Target Intraocular Pressure (Target IOP)
Therapy in glaucoma management aims to lower IOP to slow the rate of visual field
deterioration.
Target IOP is the upper limit of the IOP estimated to be compatible with a rate of
progression sufficiently slow to maintain vision-related quality of life in the expected
lifetime of the patient. It should be re-evaluated regularly and, additionally, when
progression of disease is identified or when ocular or systemic comorbidities
develop [II,D].
There is no single Target IOP level that is appropriate for every patient, so the
Target IOP needs to be estimated separately for each eye of every patient (See
FC IX and X) [II,D].
FC IX - Considerations on Target IOP
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134
Factors to consider when setting the Target IOP include19, 28, 46 [II,D]:
% Stage of glaucoma
o The greater the pre-existing glaucoma damage, the lower the Target IOP
should be
% IOP level before treatment
o The lower the untreated IOP levels, the lower the Target IOP should be
% Age and life expectancy
o Whilst younger age implies greater life expectancy and, therefore, a lower
Target IOP, older age is a risk factor for more rapid progression
% Rate of progression during follow-up
o The faster the rate of progression, the lower the Target IOP should be
% The presence of other risk factors, e.g., exfoliation syndrome
% The side effects and risks of treatment
% Patient preference
When taking the IOP reading, it is advisable to consider CCT [I,C].
Several clinical studies have identified that worse initial visual field loss is the most
important predictor of blindness from glaucoma7, 47-49. When considering the Target
IOP for one eye, the vision status of the other eye should be taken into account.
In a newly-diagnosed patient, the rate of progression is unknown and Target IOP is
based on risk factors for progression (See Ch. 2.2.2.1). After sufficient follow-up and
with sufficient visual field tests to reliably determine the progression status, usually
2-3 years, the importance of the risk factors for decision-making decreases and
importance of the measured rate of progression increases; the rate of progression
should be used to adjust the Target IOP, taking into account IOP levels over the
observation period, life expectancy, and current levels of visual function damage
(See FC X)22.
135
3.2.1.1 Setting the Target IOP
There is little evidence base to support any particular algorithm to set the Target IOP,
but data from clinical trials may be used as a guide. As clinical trials have shown
that progression occurs in eyes that have an IOP within the statistically normal range
(<21 mmHg), older recommendations that treated IOP should be simply within the
statistically normal range are no longer regarded as sufficiently ambitious.
In newly diagnosed patients, the Target IOP is initially determined according to
stage of disease and the starting IOP, with the treatment goal being a specific IOP
level or a percentage reduction, whichever is the lower50 [II,D]. For instance, in early
glaucoma, an IOP of <21 mmHg with a reduction of at least 20% may be sufficient.
In moderate glaucoma, an IOP <18 mmHg with a reduction of at least 30% may be
required [II,D]. Lower Target pressures may be needed in more advanced disease
[I,D]. The Target IOP based on stage of disease and IOP then needs to be refined
according to the presence of other risk factors, expected longevity of the patient,
the burden of therapy and the patient preferences (See FC X)46 [II,D].
FC X - Setting the Target IOP
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136
3.2.1.2 Achieving the Target IOP
Initial therapy may be with topical medication or laser trabeculoplasty [I,A]. The principles
of adjusting therapy to achieve treatment targets are shown in Flow Charts IX - X - XI.
To minimize side effects, the least amount of medication required to achieve the desired
therapeutic response should be given. If a patient fails to attain the Target IOP during
follow-up, and additional therapy is being considered, then the Target IOP should be
reaffirmed to ensure that it is still appropriate [II,D].
FC XI - Adjustment of Target IOP
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137
3.2.1.3 Re-evaluating Target IOP
If the visual field is worsening at a rate that may threaten Quality of Life during the
patient’s expected lifetime, then the Target IOP, if previously met, should be lowered;
a further 20% reduction has been shown to be effective51. If the Target IOP had not
previously been met, then additional therapy should be considered, in consultation
with the patient, weighing the risks and benefits of the additional intervention (See
FC XI) [I,D].
If there are sufficient visual fields to judge the rate of progression, and this rate is
sufficiently slow not to impact on the patient’s quality of life, then the Target IOP may
be revised upward if the Target IOP has not been met or if the patient is on excessive
therapy or is experiencing side effects [II,D].
If there are insufficient visual fields to judge the rate of progression and the Target IOP
has not been met, then additional therapy should be considered, as above [II,D].
FC XII - Considerations on First Choice Treatment
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138
3.3 - ANTIGLAUCOMA DRUGS

Several prospective randomized multi-centre controlled clinical studies have clearly
established the benefits of IOP reduction in managing POAG at various stages of the
disease whether of the ‘high pressure’ or ‘’normal pressure’ variety as well as reducing
the conversion of OHT to POAG10,18,28,52-56 [I,A].
Most forms of open-angle glaucoma and many types of chronic angle-closure glaucoma
are initially treated with topical and occasionally orally administrated agents that act either
on the reduction of aqueous humour production or enhancement of the aqueous outflow
or on both. An uncommon exception to initiating treatment with medical therapy is for
eyes with a very high level of IOP at presentation causing an immediate threat to sight.
Additionally many forms of childhood glaucoma are managed with early surgery [I,D].
Although acute angle closure with or without glaucoma needs rapid laser or incisional
surgery, medical treatment usually will be initiated as a first step in most cases.
Laser treatment may be a suitable first option for patients with known intolerance or
allergy to topical agents or suspected poor compliance [I,A].
When initially selecting medical therapy it is important to consider some relevant patient’s
characteristics as well as features related to the drug (See FC XII and XIII).
FC XIII - Medical Management - Choosing Therapy
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3.3.1. Start with Monotherapy
It is recommended to initiate the treatment with monotherapy (See FC XIII - XIV) [II,D].
Treatment is considered “effective” when the achieved IOP reduction on treatment
is comparable to the published average range for that drug in a similar population.
According to a meta-analysis of randomised controlled trials, the highest reduction
of IOP is obtained with prostaglandins, followed by non-selective b-blockers, alpha-
adrenergic agonists, selective b-blockers and at last topical carbonic anhydrase
inhibitors57.
It should be noted, however, that treatment effects depend on baseline IOP, with larger
reductions in patients with higher pre-treatment pressure levels. At low IOP values
medical and/or laser therapy have smaller effect on IOP. Therefore, when evaluating the
efficacy of a therapy or a drug it is important to consider the pre-treatment baseline
IOP58.
If this initial therapy reduces IOP to the target and is well tolerated, therapy can be left
unchanged, but the patient needs to be monitored with regular checking of endpoints [I,D].
FC XIV - Therapeutical Algorithm in Glaucoma

Topical Therapy
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140
3.3.1.1 Switch to Another Monotherapy
If the initial therapy does not seem effective, with the target pressure not being reached,
or the drug is not tolerated, one should switch to another monotherapy rather than
adding a second drug [II,D]. This applies also to prostaglandin analogues, (PGA) when
used as first choice. As there are non-responders to certain PG analogues the switch to
another PGA or another class of monotherapy might be of benefit [II,D]. Laser therapy
may also be a therapeutical option (See FC XIII) [I,A].
3.3.1.2 Add Second Drug / Combination Therapy
If the first choice monotherapy is well tolerated and has effective IOP lowering
but has not succeeded in reaching the target pressure, the addition of a second
drug should be considered [II,D]. While individualizing adjunctive therapy, issues
to consider in selecting an adjunctive agent include additive efficacy, safety,
frequency of dosing and cost. It is recommended to combine agents with different
modes of action, one that affects production of aqueous humour and another
that influences outflow [II,D]. In general, treatment with a combination of agents
of different classes is associated with superior IOP lowering efficacy compared
to each of the components used alone [I,A] (see Tables 3.1-3.2). However poly-
drug regimens for glaucoma pose several important clinical challenges: multiple
topical treatments may jeopardize adherence 59,60, result in reduced efficacy through
wash-out of earlier medications with later medications 61,62 and increase exposure
to preservatives 63, 64.
Therefore, fixed combination therapy, when available, should be preferable to two
separate instillations of agents [I, B].
Currently, all fixed combinations available in Europe contain a beta-blocker.
However, beta-blocking agents can be associated with systemic side effects and
need to be used cautiously in patients with serious concomitant cardiopulmonary
diseases. It is therefore mandatory to exclude patients with these contra-indications
before prescribing fixed combinations [I,D]. It is not recommended to combine two
bottles of fixed combinations as both will contain a `-blocker and double the
amount of this active drug with the risk of more systemic side effects [I,D]. On the
other hand, fixed combinations containing timolol may be associated with a better
local tolerability in some patients, though data are limited 65.
Fixed combinations usually have clinical equivalence to unfixed combinations;
slight differences in IOP-lowering efficacy may be seen in some cases 66,67.
Occasionally IOP-lowering agents are available as fixed combinations in some
countries and are in development in others. A new fixed combination without a
`-blocker, containing a carbonic anhydrase inhibitor (brinzolamide 1.0%) and an alpha
2 adrenergic receptor agonist (brimonidine tartrate 0.2%) has been recently approved
by the FDA and submitted to EMEA but is not yet widely available. Also, a new fixed
combination of tafluprost 0.0015% and timolol 0.5% has been submitted to EMEA.
Combination therapy, either as poly-drug regime or as fixed combination, is not
recommended as first-line treatment [II,D]. However, in selected cases, such as
advanced glaucoma and/or very high levels of IOP, the requested IOP reduction
141
may exceed the efficacy range that can be expected by a single agent. Therefore,
although the standard treatment algorithm remains unchanged, the time inter val
between incremental therapeutic steps may be decreased, combination therapy, fixed
or unfixed, can be adopted more quickly than usual or even immediately [II,D].
If combination therapy fails to lower IOP sufficiently, one can either substitute the
second drug or add a third medication to the fixed combination. At this stage however
laser or incisional surgery, if possible, should be considered [II,D].
Table 3.1
Combined IOP-lowering topical medications
Bimatoprost 0.03% Timolol 0.5%
Latanoprost 0.005% Timolol 0.5%
Travoprost 0.0004% Timolol 0.5%
Brimonidine 0.2% Timolol 0.5%
Dorzolamide 2% Timolol 0.5%
Pilocarpine 2% Timolol 0.5%
Pilocarpine 4% Timolol 0.5%
Pilocarpine 2% Metipranolol 0.1%
Pilocarpine 2% Carteolol 2%
Brinzolamide 1% Brimonidine 0.2%
Tafluprost 0.0015% Timolol 0.5%
Table 3.2
DRUG COMBINATIONS - ADDITIVE EFFECT
ADDITIONAL DRUG
CURRENT DRUG
Prostaglandin/
Alpha2-agonists Beta-Blockers Topical CAIs Cholinergic
Prostamides
Alpha2-agonists + + + +
Beta-Blockers + + + +
Topical CAIs + + + +
Cholinergic + + + +/-
Prostaglandin/ Prostamides + + + +/-
142
3.3.2 The Effect on IOP
The pre-post IOP graph shown below is a useful tool to show the IOP changes induced
by treatment and its use should be encouraged in publications.
15 21
ct
30 fe
ef
No
4
21
Post IOP
20 3
1 1
2
2 4
15
3
10
mmHg 10 20 30
Pre IOP
Figure 3.2. The Pre - Post IOP Graph.

A simple graph can be used to show the IOP lowering effect. Different shapes/colours can be used
to show different patient series or different observation times. Vertical and horizontal lines show
respectively Pre and Post Treatment IOP levels of interest, here placed as examples at 15 and
21 mmHg. Areas of desired effect under the oblique “no effect” line can thus be defined.
Treatment “A” blue dots: eye n 1 lies on the “no effect” line. Eyes n 2 and n 3 both show a large
effect, with only the former below the 15 mmHg line. Eye n 4 shows a sizeable decrease of IOP but
the absolute level is still >21 mmHg.
Treatment “B” red dots. Eyes n 1 and n 2 show a slight increase and a slight decrease of IOP, respectively;
eye n 3 shows a very large effect, as well as eye n 4, both remaining below the 15 mmHg line.
143
REMEMBER: [I,D]
* Assess each eye individually when deciding the most appropriate therapy.
* It is essential to involve patients as informed partners in decisions regarding the

management of their condition.
* The least amount of medication (and consequent inconvenience, costs and side
effects) to achieve the therapeutic response should be a consistent goal.
* A therapeutic medical trial on one eye first can be useful to determine the IOP
lowering efficacy, although not always logistically feasible or advisable (e.g., very
high IOP or advanced disease).
* Usually there is no need to start treatment until all baseline diagnostic data are
collected, unless the IOP is very high and there is severe damage.
* After diagnosis it is advisable to measure untreated IOP more than once before
initiating IOP-lowering treatment
The following pages outline the most frequently used anti-glaucoma medications, and
emphasize their mode of action, dosage and side effects. A complete list of all possible
medications is beyond the scope of the Guidelines.
144
Antiglaucoma drugs have been available since 1875. The following diagram shows
the chronology of the introduction of topical intraocular pressure-lowering medications
(Fig. 3.3).
bimatoprost/ FC bimatoprost/ FC brimonidine/

travaprost timolol brinzolamide
FC dorzolamide/ FC latanoprost/ FC travaprost/ FC timolol/
pilocarpine timolol dorzolamide timolol timolol timolol tafluprost
1875 1925 1978 1992 1994 1996 1998 2000 2001 2005 2006 2008 2014
epinephrine FC pilocarpine/ latanoprost brinzolamide FC timolol/ FC brinzolamide/

timolol brimonidine brinzolamide timolol
tafluprost
Systemic carbonic anhydrase inhibitors are available since 1955
Figure 3.3. IOP lowering molecules and year of first clinical use. FC: fixed combination. In black:
monotherapy.
There are six classes of topical antiglaucoma drugs. The following tables contain only
the most common classes and compounds, their most common side effects and
contraindications. They are listed in order of first and second line drugs.
The seventh category is systemically administered osmotics.
The use of some compounds like epinephrine and dipivefrin has decreased significantly
since drugs with better efficacy and fewer side effects became available.
The text should be considered as a general guide, and cannot be all-inclusive.
145
3.3.3 First Line Drugs
Table 3.3 Class: PROSTAGLANDIN ANALOGUES
Mode of IOP Contra-

Compound Side effects
action reduction indications
Local: Conjunctival
Latanoprost hyperaemia, burning
0.005% stinging, foreign body
sensation, itching,
Increase in increased pigmentation
Tafluprost
Prostaglandin uveo-scleral of periocular skin,
0.0015% 25-35%
analogues outflow periorbital fat atrophy,
Travoprost eyelash changes.
0.003% - Increased iris
0.004% pigmentation, (in
green-brown, blue/
Contact
grey-brown or
lenses (unless
yellow-brown irides).
reinserted 15
Cystoid macular
minutes following
oedema (aphakic/
administration of
pseudophakic patients)
the drugs)
with posterior lens
Bimatoprost capsule rupture or in
0.03% Increase in eyes with known risk
uveo-scleral factors for macular
Prostamide 25-35% oedema, reactivation of
Bimatoprost outflow
0.01% herpes keratitis, uveitis
Systemic: Dyspnea,
chest pain/angina,
muscle-back pain,
exacerbation of asthma.
146
Table 3.4 Class: Beta-RECEPTOR ANTAGONISTS

Mode of IOP Contra-
Compound Side effects
action reduction indications
Local: Conjunctiva
hyperaemia, SPK, dry
Timolol eye, corneal anesthesia,
0.1-0.25-0.5% allergic blepharo-
conjunctivitis
Levobunolol Systemic: Bradycardia,
0.25% Asthma, history arrhythmia, heart
Decreases of COPD, sinus failure, syncope,
Metipranolol aqueous bradycardia bronchospasm, airways
Nonselective 20-25%
0.1-0.3% humour (< 60 beats/min), obstruction, distal
production heart block, or oedema, hypotension,
Carteolol cardiac failure Hypoglycemia may
0.5-2.0% be masked in Insulin
dependent Diabetes
Befunolol Mellitus (IDDM),
0.5% nocturnal systemic
hypotension, depression,
sexual dysfunction
Local: Burning, stinging
more pronounced than
Asthma, history with non-selective
Decreases of COPD, sinus compounds
Beta-1- aqueous bradycardia (< 60 Systemic: Respiratory
Betaxolol 0.5% ±20%
selective humour beats/min), heart and cardiac side effects
production block, or cardiac– less pronounced than
coronary failure with non-selective
compounds, depression,
erectile dysfunction
147
Table 3.5 Class: CARBONIC ANHYDRASE INHIBITORS

Mode of IOP
Compound Contra-indications Side effects
action reduction
Local: Burning,
stinging, bitter taste,
superficial punctate
Patients with low keratitis, blurred vision,
Decreases
Brinzolamide 1% corneal endothelial tearing
aqueous
Topical 20% cell count, due to
humour Systemic: Headache,
Dorzolamide 2% increased risk of
production urticaria, angioedema,
corneal oedema
pruritus, asthenia,
dizziness, paresthesia
and transient myopia.
Systemic:
Depressed sodium
Paresthesias, hearing
and/or potassium
dysfunction, tinnitus,
blood levels,
Acetozolamide loss of appetite, taste
Decreases cases of kidney
alteration nausea,
aqueous and liver disease
Systemic Methozolamide 30-40% vomiting, diarrhoea,
humour or dysfunction,
depression, decreased
production suprarenal
Dichlorphenamide libido, kidney stones,
gland failure,
blood dyscrasias,
hyperchloremic
metabolic acidosis,
acidosis.
electrolyte imbalance
148
Table 3.6 Class: Alpha-2 SELECTIVE ADRENERGIC AGONISTS

IOP
Compound Mode of action Contra-indications Side effects
reduction
Local: Lid retraction,

Apraclonidine Decreases aqueous
25-35% conjunctival
0.5-1.0% humour production
blanching,
limited mydriasis
Decreases aqueous (apraclonidine),
Brimonidine humour production allergic
0.2% and increases blepharoconjuntivitis,
uveo-scleral outflow periocular contact
dermatitis, allergy
Oral monoamine or delayed
oxidase (MAO) hypersensitivity
Alpha-2- inhibitor users (apraclonidine
selective Pediatric age and clonidine
Very low body weight >brimonidine)
18-25% in adults
Systemic: Dry
Clonidine
Decreases aqueous mouth and nose
0.125
humour production (apraclonidine).
-0.5%
Systemic
hypotension,
bradycardia
(clonidine),
fatigue, sleepiness
(brimonidine)
149
3.3.4 Second Line Drugs
Table 3.7 Class: NON SELECTIVE ADRENERGIC AGONISTS
IOP
Compound Mode of action Contra-indications Side effects
reduction
Local: Conjunctival
hyperemia,
conjunctival
pigmentation. Burning,
stinging, ocular pain,
Epinephrine Decreases aqueous Occludable angles blurred vision, macular
Non- 0.25-2.0% humour production (iridotomy needed) oedema
15-20%
selective and may increases Aphakic patients
Dipivefrin 0.1% uveo-scleral outflow (macular oedema) Systemic: systemic
hypertension,
headache, anxiety,
confusion, chest pain,
shortness of breath,
tachycardia, sweating
Table 3.8 Class: PARASYMPATHOMIMETICS (CHOLINERGIC DRUGS)
Mode of IOP
action reduction
Post-operative Local: Reduced vision
inflammation, due to miosisand
Facilitates
uveitis neovascular accommodative
aqueous
glaucoma. Patient myopia, conjunctival,
outflow by
at risk for retinal hyperaemia, retinal
Pilocarpine contraction
detachment, spastic detachment, lens
0.5-4% of the ciliary
Direct- gastrointestinal opacities, precipitation
muscle, tension 20-25%
acting disturbances, peptic of angle closure, iris
Carbachol on the scleral
ulcer, pronounced cysts
0.75-3% spur and
bradycardia,
traction on
hypotension, Systemic:
the trabecular
recent myocardial Intestinal cramps,
meshwork
infarction, epilepsy, bronchospasm,
Parkinsonism headache
Demecarium
bromide
0.125-0.25%
Local and systemic:
Side effects are similar
Indirect- Ecothiophate Same as direct acting
15-25% but more pronounced
acting iodide 0.03% drugs
than with direct acting
compounds
Diisopropyl
fluorophosphates
0.025-0.1%
150
Table 3.9 OSMOTICS

Mode of IOP
action reduction
Nausea, Vomiting,
dehydration (special
Glycerol Dehydration
caution in diabetic
and reduction
patients). Increased
Oral Isosorbide in vitreous 15-20% diuresis, hyponatremia
volume
when severe may lead
Alcohol Posterior Cardiac or renal
to lethargy, obtundation,
movement of failure
seizure, coma.
the iris-lens
Possible increase of
plane with
Mannitol bood glucose.
deepening of
Intravenous 15-30% Acute oliguric renal
the AC
Urea failure. Hypersensitivity
reaction
3.3.4.1 Prostaglandin Analogues
Since their development in the 1990s, prostaglandin derivatives (latanoprost, travoprost,

bimatoprost and tafluprost) (Table 3.3) have progressively replaced beta-blockers as
first-choice/first line therapy. This is mainly because they are the most effective IOP-
lowering agents 54, lack relevant systemic side effects and require just once-daily
administration. Recently, a number of latanoprost generics as well as preservative-free
and BAC-free prostaglandin formulations have entered the glaucoma market.
The primary mechanism of action of prostaglandins is to increase uveoscleral outflow,
reducing IOP by 25%-35%. Reduction of IOP starts approximately 2-4 h after the
first administration, with the peak effect within approximately 8-12 h. Thus, IOP
measurements taken in the morning represent the peak effect of the prostaglandin
analogues for patients administering the drug in the evening. Clinical trials that
measured 24-hour IOP suggested that evening administration is generally preferable
because it gave a better circadian IOP profile 68-70 [II, B]. These studies also reported
that eyes treated with PG derivatives have reduced short-term IOP variability as
compared to eyes treated with other classes of drugs71.
Maximum IOP lowering is often achieved 3-5 weeks from commencement of
treatment. Differences among drugs within this class in the capability of reducing
IOP did not exceed 1 mmHg72. When combined with most of the other antiglaucoma
drug classes, prostaglandin agents provide additive IOP lowering.
Non-responders to prostaglandin analogues (e.g. eyes with IOP reductions of less
than 10% or 15% from baseline) are fewer than 10%73,74. Some reports indicate that
poor responders to one prostaglandin agent might respond to another agent within
the same class75,76. Conjunctival hyperemia, generally mild, is a common finding
with slight difference in frequency and level among agents within this drug class.
It usually decreases over time. Other PG side effects are reported in Table 3.3.
Details on the mode of action, IOP lowering effect, contraindications and side
effects of other first line drugs (`-blockers, carbonic anhydrase inhibitors, alpha-2
selective adrenergic agonists) and second line drugs are listed in Tables 3.5-3.10.
151
3.3.5 Local Toxicity of Topical IOP - Lowering Treatment. The Role of

Preservatives
Long-term topical glaucoma medications may cause and/or exacerbate pre-existing

ocular surface disease (OSD), such as dry eye, meibomian gland dysfunction and chronic
allergy77, which, in glaucoma patients, has a much higher prevalence than in the general
population63,64,78. OSD may follow chronic use of antiglaucoma medication and/or the
preservative benzalkalonium chloride (BAC). BAC, a quaternary ammonium compound is
the most frequently used preservative agent in eye drops and its usage correlates well
with the signs and symptoms of OSD63, 64,79-82. Such signs and symptoms can diminish
if BAC-preserved drops are substituted with non-preserved drops63. An unwanted effect
of BAC is a reduction in the success rate of filtering surgery83-85. In vitro studies suggest
that alternative preservatives are significantly less toxic than BAC86-91.
Other therapeutic possibilities are the use of preservative-free or BAC-free medication,
decreasing the number of preserved eyedrops i.e. by using fixed combinations;
treating the ocular surface with unpreserved tear substitutes and performing earlier
laser or surgery. When considering OSD four factors have to be considered: the active
compound, the specific preservative, the ability of the patient to use single-dose
preparations and the patient’s ocular surface.
The European Medicines Agency (EMEA) has suggested that the use of preservatives
should be avoided in “patients who do not tolerate eye drops with preservatives”
and in those on long-term treatment, or to use “concentration at the minimum level
consistent with satisfactory antimicrobial function in each individual preparation”, with
a specific indication to avoid mercury containing preparations92.
Not all patients are sensitive to preservatives and not all the local side effects
observed with topical antiglaucoma medications are induced by preservatives.
Particular attention should be paid to glaucoma patients with pre-existing OSD or
to those developing dry eye or ocular irritation over time. This can be done by
careful assessment of redness of the eyelid margin, positive corneal and conjunctival
fluorescein staining or reduced tear break-up time [I,D].
3.3.6 Generic IOP - Lowering Topical Medications
By definition a generic drug is identical to a brand name drug in dosage, strength,

route of administration, performance characteristics and intended use. For the
purposes of drug approval, the interchangeability of a generic drug and the
corresponding brand-name drug is based on the criterion of “essential similarity”.
In ophthalmology this concept is problematic, because it is difficult to prove
“essential similarity” in clinical studies. With systemic drugs bioequivalence studies
are performed using blood samples to determine whether the plasma concentration
within certain limits equals the branded drug. With topical eye drops such studies
obviously cannot be performed.
No clinical studies are usually required for generic approval in ophthalmology, and a
10% difference between the concentration of the active principle between the generic
and the branded products is considered acceptable. Whereas the active principle is
assumed to be equal, the adjuvants can vary considerably. This is a critical issue
152
because different adjuvants may alter the viscosity, osmolarity and pH of the eye
drops and therefore have an impact on both tolerability and corneal penetration.
Nevertheless anti-glaucoma generics drugs are currently prescribed at a large scale,
as many drugs are becoming off patent. For latanoprost, the generic share is more
than 65% in most European countries. To which degree these generics are similar in
efficacy and tolerability is not well studied. Only few clinical studies have compared
the effect of generic and brand IOP lowering medications in glaucoma, with variable
results depending on the type of generic drug 93,94. Other studies have shown a
difference between the branded and the generic preparations concerning the size
and amount of drops in the bottle, the structure of the bottle and the bottle tips95-98.
Safety issues with corneal epithelial disorders have also been described with generics,
due to an additional stabiliser compound99. When switching patients from branded to
generic drugs, the IOP should be closely monitored [I,D].
3.3.7 Dietary Supplementation and Glaucoma
Although there is no clinical evidence for clinical benefits arising from the use of
dietary supplements in glaucoma, a recent survey has found that 1 in 9 glaucoma
patients were using complementary and alternative medicine (CAM). Most were
using herbal medicines (34.5%), dietary modifications (22.7%) or dietary supplements
(18.8%)100. Based on the fact that some glaucoma patients continue to progress
at low IOPs, there is much room for hypotheses, preclinical experiments, clinical
trials and speculation. Some data from experimental studies suggest that dietary
supplementation may reduce oxidative stress101, or that the omega 3 polyunsaturated
fatty acids (PUFAs) decrease IOP in rats102. At the present time there is no robust
interventional dietary supplementation study demonstrating the positive effect of such
a treatment in glaucoma patients. Observational studies have suggested a reduced
risk for glaucoma with higher fruit and vegetable intake103 or higher omega 3 PUFAs
consumption in selected populations104. Conversely there is evidence that some of
these compounds may cause harm, such as an increased intake of magnesium
associated with a higher incidence of glaucoma105.
DIETARY SUPPLEMENTATION
At the present time there is no robust interventional dietary supplementation study
demonstrating the positive effect of such a treatment in glaucoma patients
3.3.8 Management of Glaucoma During Pregnancy and Breast-feeding
Pregnancy-related changes in ocular physiology can influence IOP as well as the

reliability of its measurements. Changes in hormonal levels, are thought to induce an
IOP-lowering effect that increases throughout pregnancy (but particularly during the
24th-30th week) and can last for months after delivery106-108.
The most sensitive period is the first trimester due to concerns relating teratogenicity,
153
as the majority of IOP-lowering medications are within class C (See Table 3.10)
meaning that adverse effects have been seen in animals or that there are no
human or animal data (See Table 3.11). Therefore, for a woman with glaucoma who
is of child bearing age, who might wish to conceive, the treatment strategy during
pregnancy should be discussed [I,D]. The patient should be instructed to inform
the ophthalmologist when pregnancy occurs. The potential risks to the fetus (and
neonate) of continuing anti-glaucoma medications must be balanced against the risk
of vision loss in the mother [I,D]. As IOP levels generally decrease during pregnancy,
temporary treatment discontinuation can be considered under strict follow-up
in some patients. However, if continuation of treatment is mandated, the lowest
effective dosage of medication should be used. Moreover, systemic absorption
should be reduced by punctal occlusion, eyelid closure, and blotting excess drops
away during administration109 [I,D].
Drugs are classified in Classes A to X for use during pregnancy based on a
hierarchy of estimated fetal risk (See Tables 3.10-3.11)110. Although very similar, some
countries (e.g., Sweden, Australia, the Netherlands, Switzerland, and Denmark) have
their own classification systems.
Table 3.10 Drug classification for use of drugs during pregnancy
Controlled studies show no risk. Adequate well-controlled studies in pregnant women

Class A
have failed to demonstrate risk to the foetus
No evidence of risk in humans. Either animal findings show risk, but human findings
Class B do not or, if no adequate human studies have been done, animal findings are
negative
Risk cannot be ruled out. Human studies are lacking, and animal studies are either
Class C positive for foetal risk or lacking as well. However, potential benefits may justify the
potential risk
Positive evidence of risk. Investigational or post-marketing data show risk to the

Class D
foetus. Nevertheless, potential benefits may outweigh the potential risk
Contraindicated in pregnancy. Studies in animals or human, or investigational or

Class X post- marketing reports, have shown foetal risk which clearly outweighs any possible
benefit to the patient
(FDA Classification of Drugs for Teratogenic Risk. Teratology society public affairs committee. Teratology
1994: 49:446-447).
154
Brimonidine is a Class B medication: however, there are reports of central nervous

system side effects in young children111. The ability of this drug to cross the placenta
and the lack of well controlled human studies during pregnancy do not allow ruling out
possible adverse effects on the fetus. Betaxolol is also in class B and is characterized
by a larger volume of distribution in the fetal circulation, high binding to proteins and
therefore fewer central nervous systemic effects on the fetus. Timolol although class
C, is available in low dosage (0.1%), in slow-release preparations which can be used
once daily. Although these formulations are thought to reduce systemic absorption,
strong evidence to support this is still lacking. Once-a-day timolol 0.1% gel may be
a valid option if a beta-blocker is considered [I,D]. Prostaglandin-analogues should
be considered with caution because of the theoretical risk of increased uterine
contractility in pregnancy. If premature contractions appear PG should be discontinued
immediately [I,D].
There have been no reports on any fetal complications related to the use of topical
carbonic anhydrase inhibitors in humans, but animal studies have shown that high
systemic doses, are associated with low weight offspring (Manufacturer’s Information:
Azopt product monograph. Fort Worth, Texas, Alcon Ophthalmics, 1998 Manufacturer’s
Information: Trusopt product monograph. West Point, Pennsylvania, Merck Inc., 1999).
At clinically used concentrations, BAC has no known impact on the fetus112.
Table 3.11 summarizes known adverse effects of anti-glaucoma drugs during pregnancy
and breast-feeding.
Although results from animal studies are worrisome, the overall level of evidence for the
risk of giving anti-glaucoma drugs to pregnant women is low.
Laser trabeculoplasty is considered to be a safe alternative113 except in patients with
angle dysgenesis. However, IOP lowering success is lower in younger patients, such as
in women of childbearing age114.
Laser cyclodestruction, in spite of having been suggested as a valid option should be
considered with caution because of risk of sight-threatening complications115.
If surgery is planned, there are a number of considerations to be made. A supine position
should be avoided116. For intervention under local anesthesia, topical, subconjuntival or
retrobulbar, lidocaine is considered to be a safe option117. The use of anti-metabolites is
strictly contraindicated, due to the mutagenic related risk. Depending on previous ocular
surgeries and the age of patient, filtering surgery, including tube shunt implantation, can
be considered112 [II,D].
Topical prednisolone and erythromycin have been shown to cross the placenta to a
lesser extent than other medications of their classes, and can therefore be chosen as
postoperative medication117,118 [II,D].
Special attention should be paid also during breast-feeding. Carbonic anhydrase
inhibitors and beta-blockers may be used in nursing mothers as suggested by the
American Academy of Pediatricians119. These are also the first line choices in infants
with congenital glaucoma when medical therapy is being considered.
Fixed combinations are all class C. Prescribing physicians should separately consider
each of the drugs involved [I,D].
155
Table 3.11 Adverse effects of IOP-lowering medications during pregnancy/breast-feeding

astfeeding Class Pregnancy Breast-feeding
Animal Studies Human
Theoretical risk Reported cases
Teratogenicity
Parasympathetic Meningism in Seizures, fever,
C Teratogenic Dysregulation of
agents newborn diaphoresis
placental perfusion
CNS depression,
Sympathetic agents No significant Delay in labor/ No reported
B hypotension
• brimonidine effect uterine hypotony side-effects
andapnea
Prostaglandin High incidence of Uterine One case of No reported
C
analogs miscarriage contractions miscarriage side-effects
Arrhythmia and
Teratogenicity Controversy
bradycardia
Delayed fetal (1st trimester) overconcentrations
Impaired
Beta-blockers C ossification, fetal Cardiac rhythm inbreast milk.
respiratory
resorption changes Apnea and
control in
Respiratory bradycardia
newborns
Carbonic
anhydrase
inhibitors
Decreased weight
gain Lower fetal No reported No reported
• Topical C
Vertebral body weight side-effects side-effects
malformation
Forelimb Limb Onecase No reported
• Oral C
anomalies malformations of teratoma side-effects
NOTE: there is a lack of well-controlled human studies during pregnancy. Therefore it is not possible
to accurately determine the real incidence of the stated adverse effects, or to exclude the existence of
any additional unforeseen adverse effects on the fetus.
3.3.8 Neuroprotection and Glaucoma Treatment
Neuroprotection can be defined as a “therapeutic approach” aiming to directly prevent

or significantly hinder neuronal cell damage. Since glaucoma patients can continue
deteriorating in spite of an apparently well controlled IOP, the need for effective
non-IOP related treatments is widely acknowledged. Several compounds have been
neuroprotectant in preclinical studies120. Only two have reached large scale clinical trials:
a large long-term RCT using an NMDA antagonist, memantine, was analysed in 2008
with negative results. More recently, the results from a multi-center RCT of adults with
low-pressure glaucoma (Low-pressure Glaucoma Treatment Study, LoGTS) has been
claimed to show that brimonidine may have neuroprotective properties in comparison
to Timolol44. No direct comparison has been done with other substances such as
PG. However, the authors of the study and a systematic literature review have (both?)
suggested that more substantial evidence is needed121,122.
156
3.3.9 Practical Considerations Related to Topical Medical Treatment
The majority of topically applied drugs, particularly if lipophilic, penetrate the eye via the
cornea, in a lesser amount via the conjunctiva and thereafter the sclera.
On average, the total tear film volume is around 7 μl and the rate of tear film turnover
is approximately 15% (±1 μl) per minute but can double (washout effect) after the
application of a topical drop with a volume estimated at 30-50 μl123. Although the cul-
de-sac and tear film compartment can expand transiently after instillation of a drop
it still cannot accommodate this whole volume and less than 5% manages to enter
the eye; the rest will run down the cheek or will be drained through the nasolacrimal
duct where an individually variable systemic absorption takes place through the highly
vascularised nasal mucosa124.
Once the medication is instilled into the conjunctival sac, the spontaneous tear flow will
cause complete washout within 5 minutes.
The washout effect depends not only on the increased tear fluid turnover, but also on
the addition of a second drop within a short period. Therefore when poly-drug regimen
is used, a minimum time span between different drops should be respected. When two
drugs are instilled only 30 seconds apart, almost 50% of the first drug will be washed
out. The recommended delay between drops is 5 minutes with a washout effect of less
than 15%61,62 [I,B].
Blinking also may influence washout and allow only 15% of a topically applied drug to
remain in the eye approximately five minutes after instillation.
As drugs absorbed through the highly vascularised nasal mucosa avoid hepatic first-
pass metabolism this might lead to systemic side effects. The instillation of one drop of
timolol 0.5% for example may lead to a serum concentration of timolol that equals the
intake of an oral 10 mg non-selective beta-blocker125.
There is no evidence that nasolacrimal duct obstruction may increase the efficacy
of a topical drug126 however it may reduce systemic side effects particularly from
beta-blockers by minimizing the drainage into the highly vascularised nasopharyngeal
mucosa109,127,128 [I,D].
Patients should be advised to shake the bottle before use as micro-suspensions tend to
settle to the bottom of the bottle leaving the vehicle at the surface. Thus, patients may
be simply applying mainly vehicle to the eye, rather than the active drug ingredient [I,D].
157
GENERAL RECOMMANDATIONS [l,D]:

• Monotherapy is the first choice when initiating therapy
• Baseline IOP should be considered when evaluating the efficacy of a therapy
• Fixed Combination therapy should be considered when patients fail to achieve their
individualized intraocular pressure (IOP) targets with monotherapy
• The prescription of more than two bottles of IOP lowering eye drops for simultaneous
use should be avoided as it can lead to noncompliance
• Fixed combination preparations may be preferable to the use of separate instillation
of two agents
• However Fixed Combination are not first-line medications and they are only
indicated in patients who need adjunctive therapy, when IOP is not sufficiently
controlled by one single agent
• Ocular surface should be evaluated and considered in clinical management of
glaucoma patients. In case of ocular surface disease, preservative-free formulations
should be considered
• Generic drops can differ from brand drops and it may be necessary to monitor
patients more closely after switching
• During pregnancy, the potential risks of continuing anti-glaucoma medications to
the fetus (and neonate) must be balanced against the risk of vision loss in the
mother
See FC IX to XIII
158
3.4 - ADHERENCE, COMPLIANCE AND PERSISTENCE IN GLAUCOMA

Glaucoma is a chronic progressive disease that requires continuous long-term
cooperation of the patient with the glaucoma management proposed by the doctor.
3.4.1 Terminology
The commonly used term “compliance” has been increasingly replaced in recent times
by the term “adherence”. Both are defined as the ‘cooperation of the patient with the
recommendations given by the doctor’. However, the former is more passive ("I am
taking the medication”), while the latter implies the active part of the patient in the
process (“I am taking the medication exactly as you told me”).
“Persistence” is defined as the length of time during which the patient is taking the
medication as prescribed129.
Finally three terms should be mentioned:
- “White coat compliance” means that the patient’s adherence rises a week before
the consultation and drops quickly afterwards130
- “Dyscompliance” is used when physical problems of a patient, like arthritis, lead to
difficulties in correctly applying a therapy
- “Alliance” is a special form of adherence meaning that the people around the
patient ensure the correct application of the medication131
3.4.2 Measured Adherence
Despite easier medication schemes (for example drugs which require application once-
daily) and more information for the patients about the disease, the rate of non-adherence
has remained almost the same over the last 25 years; between 30%-70%.
It is important to mention that the patients themselves overestimate their adherence and
persistence rate (GAPS)132.
3.4.3 Factors Associated with Non-Adherence
Four groups of factors encountered as common obstacles to glaucoma medication

adherence have been described133:
- Situational / environmental (for example a major event in the patients life, unsteady
life-style with many travels)
- Medication (for example costs of the drugs, side effects, complicated dosing regimen)
- Patients (for example comorbidity, poor understanding of the disease)
- Provider (for example lacking communication with the doctor)
Other influencing factors:
- Gender (men are more likely to be non adherent)
- Stage of the disease (patients with a less advanced disease tend to be less adherent)
159
3.4.4 Types of Non-Adherence
Every patient is different and there are several types of non-adherence134.
- Failure to take the medication as prescribed (including under- and overdosing,

inadequate doses and wrong timing of dosages)
- Failure to use the correct medication (including the application of the wrong
medication or the self administration of not prescribed drugs)
- Failure to apply the medication correctly (including incorrect self administration of
the medication)
- Failure to continue applying the medication (including problems with side-effects,
issue of costs and missed refills)
3.4.5 Improving Adherence
There are different ways for improving the adherence of patients. The most important
measures are informing the patient about his/her disease and finding a therapeutic
regimen which fits into the patient’s life-style135 [I,D].
Other factors which should improve adherence [I,D]:
- The therapy should be simple i.e. not more than two bottles and an application
not more than twice a day
- The patient should be instructed how to apply the drops correctly. If necessary,
hints reminders should be given like a daily routine which the patient can connect
to the application of the drops. If a patient has physical problems applying the
drops as arthritis of the fingers, the therapy should be adjusted accordingly or
switched to laser/surgery
- The doctor should inquire at every visit if the patient has side effects of the
medication and switch if necessary. A patient who complains about side effects is
usually not adherent to therapy.
The patient’s cooperation, described as adherence and persistence, with the

prescribed glaucoma management is mandatory to obtain effective IOP lowering
and to prevent glaucoma progression. No drug can work unless it is taken.
160
3.5 - LASER SURGERY
3.5.1 Laser Iridotomy136-139
Indications: [I,C]
Clinically relevant or suspected pupillary block.
Potential prevention of acute and chronic angle closure (See FC X and XI).
Preoperative preparation:
To reduce iris thickness and facilitate perforation instil 1 drop of Pilocarpine 2%-4% [I,D].
If the cornea is edematous, like acute angle closure, use topical glycerin 10% if available,
systemic acetazolamide, intravenous mannitol or oral hyperosmotic agents (See FC XI).
For prevention of IOP spikes use topical alpha 2 agonist 1 hour prior to the procedure
and immediately afterwards [I,B].
Procedure:
After instillation of topical anesthetic a contact lens with contact lens fluid is placed
onto the cornea. The lens keeps the eyelids open, stabilizes the eye, provides additional
magnification, focuses the laser beam and acts as a heat sink.
Lenses used are: Abraham (+66 diopters), Wise (+103 diopters) or CGI©LASAG CH lens.
Iridotomy site [II,D] is usually chosen in the superior quadrants of the iris well covered
by the upper eyelid (to reduce visual symptoms), in a thin looking area or an iris crypt.
Whole thickness perforation of the iris is assumed when pigment, mixed with aqueous,
flows from the posterior into the anterior chamber. Once a full thickness hole has
been made, it should be enlarged horizontally to achieve an adequate size. Iridotomy
size [II,D] should be sufficient for patency inspite of iris oedema, pigment epithelial
proliferation and pupil dilation. Transillumination through the iridotomy is not a reliable
indicator of success [II,D].
Lasers parameters for Nd:YAG laser iridotomy
Power 1-6 mJ
Spot size 50-70 μm (constant for each laser model)
Pulses per burst 1-3
Set defocus to zero

Focus the beam within the iris stroma rather than on the surface of the iris*
Avoid any apparent iris vessels
Recommendations
Use the least amount of energy that is effective139
Lens capsule damage is possible above 2 mJ energy
With most Lasers less than 5 mJ per pulse is required
* Pretreatment with argon laser to minimize bleeding by coagulating iris vessels is optional (spot size
400 μm, duration 0.2 sec, energy approximately 200-300 mW).
161
In case of thick dark irides, to reduce total Nd:YAG energy, pretreatment with argon
laser in 2 stages may be considered141 [II,B]. In the first stage a low power argon of
90-250 mW, duration 0.05 sec, spot size 50mm is applied, followed by the high power
argon of 700 mW, duration 0.1 sec, spot size 50 mm to create a punched-out crater
appearance. Laser iridotomy is completed with Nd:YAG laser.
Laser parameters for continuous-wave Argon laser iridotomy

When no Nd:YAG laser is available, Argon laser may be used [II,D].
Laser parameters should be individualized to each patient and adjusted appropriately
during the procedure.
The following parameters are suggested [II,D]:
Medium brown irides
Preparatory stretch burns
Spot size 200-500 μm
Exposure time 0.2-0.6 sec
Power 200-600 mW
Penetration burns [II,D]
Spot size 50 μm
Exposure time 0.1-0.2 sec
Power 700-1500 mW (average 1000 mW)
Pale blue or hazel irides
1st step: to obtain a gas bubble
Spot size 50 μm
Exposure time 0.5 sec
Power Up to 1500 mW
2nd step: penetration through the gas bubble
Spot size 50 μm
Exposure 0.05 sec
Power 1000 mW
Thick, dark brown irides

(chipping technique)
Spot size 50 μm
Exposure time 0.02 sec
Power 1500 mW
162
Complications:
% Intraoperative complications
Bleeding from the iridotomy site; this can usually be stopped by gentle pressure
applied to the eye with the contact lens. With the argon laser corneal epithelial and/
or endothelial burns may develop.
% Postoperative
Visual disturbances occur in 6-12% (glare, blurring, ghost images, halo, crescent)
are less likely to occur when the iridotomy is completely covered by the eyelid142, 143.
Transient elevation of the IOP is the most common complication in the early period.
Elevation of IOP at 1 hour after iridotomy occurs in approximately 10% of primary angle
closure suspect eyes144. Acute and (chronic) rise in IOP is more likely to occur in eyes
with peripheral anterior synechiae in whom the small amount of trabecular meshwork
not closed is likely to have compromised outflow function (and is secondarily closed by
the iris pigment and tissue generated by the iridotomy).
Postoperative inflammation is transient and mild, rarely resulting in posterior synechiae.
Closure of the iridotomy may occur during the first few weeks after the procedure, due
to accumulation of debris and pigment granules.
Rare complications include sterile hypopyon, cystoid macular oedema, retinal
haemorrhages and malignant glaucoma145,146.
Postoperative management:
Check the IOP after 1-3 hours [II,D].
Topical corticosteroids for 4-7 days instilled 3-4 times a day.
Check the angle regularly with gonioscopy, and the patency of peripheral iridotomy.
If the patency is uncertain check with gonioscopy, reconsider the mechanism, perform
ultrasound biomicroscopy (UBM) / anterior segment-optical coherence tomography
(AS-OCT) if available and/or repeat the iridotomy.
Retroillumination alone for judging the patency is insufficient.
163
3.5.2 Laser Trabeculoplasty (LT)147-154
Indications: [I,D]
Lowering of IOP in primary open-angle, exfoliative and pigmentary glaucoma, high risk
ocular hypertension (OH):
1) When IOP is not satisfactorily controlled with medications (i.e. efficacy, tolerability
and adherence)
2) As initial treatment (See FC VII)
Preoperative preparation: [I,B]

For prevention of IOP spikes instillation of topical alpha 2 agonist (apraclonidine 1% or
brimonidine) 1 hour prior to the procedure and immediately afterwards is optional. Use
topical anesthesia.
Procedure:
Most frequently used lasers are:
- Argon continuous-wave laser (green or blue/green) - argon laser trabeculoplasty
(ALT)
- Q-switched, short pulsed, frequency–doubled Nd:YAG (532 nm) laser - selective
laser trabeculoplasty (SLT)
Lenses: Goldmann type gonioscopy lens, Ritch trabeculoplasty lens©, CGA©, Meridian,
Latina (SLT), Magnaview.
Identify angle landmarks after inspection of all quadrants and place the laser burns
between the anterior pigmented trabecular meshwork (TM) and the non-pigmented
trabecular meshwork over 180° or 360°.
164
Laser parameters for laser trabeculoplasty

Laser parameters [I, D] ALT SLT
Spot size 50 μm 400 μm
Exposure 0.1 sec 3 nsec (fixed)
500-1200 mW according to the 0.4 to 1.2 mJ according to the
Power reaction on the TM; with heavily desired reaction; in heavily pigmented
pigmented TM low power is sufficient TM start with low levels e.g. 0.4 mJ
The power is titrated until the
appearance of tiny air bubbles,
Transient bleaching or small »champagne bubbles«, at the site
Optimal reaction
gas bubble formation of the laser burn, then the power is
reduced by increments of 0.1 mJ until
there are no visible bubbles*
50-100 evenly spaced 50-100 non-overlapping spots
Number of spots
spots over 180-360° spaced over 180 -360°
* some continue with the power that causes champagne bubble formation
Complications:
Transient elevation of IOP155,156
Inflammation (mild)
Peripheral anterior synechiae (after ALT)
Corneal endothelial damage in corneas with pigment on endothelium (after SLT)157.
Post-operative management: [II,D]

Check IOP in selected patients (e.g. with advanced glaucomatous damage, one-
eyed patients, high pre-laser IOP, exfoliation syndrome, heavily pigmented trabecular
meshwork). Use of topical corticosteroids or non-steroidal anti-inflammatory medication
3-4 times daily for 4-7 days.
Effectiveness of laser trabeculoplasty:

ALT and SLT have the same efficacy153,158.
Laser trabeculoplasty is initially effective in 80 to 85% of treated eyes with a mean IOP
reduction of 20 to 25% (of 6 to 9 mmHg). The effect wears off over time, for both ALT
and SLT159.
LT versus medication: In the Glaucoma Laser Trial, after 7 years of follow-up, patients
with ALT had lower IOP (1.2 mmHg) than patients on medical treatment, and no
difference in progression of glaucoma160. SLT has shown to decrease IOP to a degree
similar to that of prostaglandin analogues after 9 to 12 months follow-up161 and appears
to be repeatable (30,31).
Predictors of efficacy:
Higher baseline IOP is associated with greater IOP reduction after SLT and ALT162,163.
The effectiveness of ALT is influenced by the treating surgeon, and success is better
when surgeons have more experience in ALT163,164.
Pigmentation of the trabecular meshwork (TM) is important. ALT is less successful in
eyes with no pigmentation of TM. SLT seems to be independent of the pigmentation of
TM. Younger subjects (less than 40 years old) usually respond less to ALT165.
165
3.5.3 Laser Iridoplasty166,167
Main Indication: [II,D]

Plateau iris syndrome confirmed by a patent iridotomy; the purpose is to enlarge the
peripheral angle approach after iridotomy, to decrease the chance of progressive
synechial closure.
Lasers:
Different types of continuous wave lasers can be used for photocoagulation, most
frequently: argon laser, diode laser (810 nm), and the frequency-doubled Nd:YAG laser
(532 nm).
Preoperative preparation: [II,D]

Instillation of Pilocarpine followed by the same preoperative preparation as for laser
trabeculoplasty.
Lens: Abraham (+66 diopters), Wise (+103 diopters), CGI©LASAG CH lens or the central
non-mirrored part of the Goldmann lens.
Contraindications: [I,D]
Flat anterior chamber
Extensive peripheral anterior synechiae.
Laser parameters [II,D]

Laser parameters [II,D] Contraction burns (long duration-low power-large spot size)
Spot size 200-500 μm
Exposure 0.3-0.6 sec
Power 200-400 mW
Location Aiming beam should be directed at the most peripheral part of the iris
Visible contraction of the peripheral iris with flattening of the iris curvature
Optimal reaction
(without bubble formation or pigment release)
20-24 spots over 360° leaving 2 beam diameters between each spot and
Number of spots
avoiding visible radial vessels
Complications:
Mild iritis
Corneal endothelial burns
Transient elevation of IOP
Post-operative synechiae of the pupil
Permanent pupil dilation
Iris atrophy
Non-dilatable pupil
Post-operative management:
Topical corticosteroids or non-steroidal anti-inflammatory medication instilled for
4-7 days
Prevention of IOP spikes
166
3.5.4 Cyclophotocoagulation168-170
Indications: [II,D]
When filtration surgery or tubes are likely to fail, have failed, or are not feasible
As an alternative to drainage devices
Lasers used:
Diode laser (810 nm); Argon laser
Modes of laser delivery are: trans-scleral, endoscopic and transpupillary
Trans-scleral cyclophotocoagulation:
Laser diode cyclophotocoagulation with the G probe is the cyclodestructive procedure
of choice because of the reduced incidence of complications compared with other
cyclodestructive procedures [I,D].
Ultrasonic cyclodestruction:
Ultrasonic circular cyclocoagulation using high-intensity focused ultrasound delivered by
a circular miniaturized device was reported as a safe and effective technique to reduce
intraocular pressure in patients with refractory glaucoma171,172.
Technique: [II,D]
Transcleral cyclophotocoagulation with diode laser and G probe
Retrobulbar or peribulbar injection of a 50:50 mixture of 2% lidocaine and

Anesthesia
0.75% bupivicaine with hyaluronidase
The G probe footplate is placed on the conjunctiva with the short side
adjacent to the limbus, which positions the fiberoptic tip 1.2 mm behind
G probe positioning the limbus. The ciliary body should be identified with transillumination
as its position may vary and the placement of the G probe is adjusted
accordingly173
The fibre optic light source is directed approx. 4 mm posterior to

Scleral transillumination corneoscleral limbus to identify ciliary body by transillumination. The dark
demarcation line indicates the anterior margin of the ciliary body
Recommended setting: duration of 2 sec., from 1500 mW for dark to

2000 mW for light-coloured irides and increase the energy until an audible
Settings »pop« is heard indicating tissue disruption. If a »pop« sound occurs during
two sequential subsequent laser applications, the power is reduced by
150 mW and treatment completed at this power174
10-20 over 180°, energy 5-6 J per pulse, total treatment per session up
to 270° of circumference avoiding 3 and 9 o'clock positions (to avoid long
Applications posterior ciliary nerves). Some surgeons prefer to use low energy and
more applications. Retreatments are often needed, but the incidence of
severe complications is low [II,D].
167
Endoscopic cyclophotocoagulation:
Endoscopic techniques combined with laser technology allow the photocoagulation of
ciliary processes not visible via the transpupillary route. The approach can be limbal
or through pars plana. Recently, endoscopic cyclophotocoagulation is most commonly
performed in conjunction with cataract surgery in cases with early glaucoma175.
Transpupillary cyclophotocoagulation:
This procedure is limited to eyes in which a sufficient number of ciliary processes can
be visualized gonioscopically, as in cases of aniridia, through a large surgical iridectomy
or when broad anterior synechiae cause anterior displacement of the iris.
New technology using ultra-sound cyclodestruction is currently under investigation.
Complications:169,176
% Rates of complications are higher in neovascular glaucoma and with treatment
protocols using more than 80 J per session.
% Persistent inflammation
% Hyphaema
% Corneal decompensation
% Vision loss
% Hypotony and phthisis
Post-operative management: [II,D]

Consider analgesia. Topical corticosteroids and atropine instillation for 2-3 weeks.
In the immediate postoperative period IOP should be monitored and the anti-glaucoma
medication tapered accordingly.
The effectiveness of treatment is assessed after 4 weeks.
168
3.6 - INCISIONAL SURGERY
3.6.1 General Principles
The different techniques of incisional surgery have different indications depending on

the type of glaucoma. Their adoption depends on: [I,D]
1. the target IOP chosen for the individual situation
2. the previous history (surgery, medications, degree of visual field loss)
3. the risk profile (i.e. single eye, occupation, refractive status)
4. the preferences and experience of the surgeon
5. the patient opinion, expectation and postoperative compliance
The decision to recommend glaucoma surgery should be made in the light of published
clinical trials54,177. In the individual patient, a multitude of factors must be taken into
account when deciding treatment including compliance, stage of glaucoma etc.
Nevertheless, surgery should be considered whenever medical or laser treatment would
appear unlikely to maintain sight in the glaucomatous eye [I,D]. It should not be left as
a last resort (See Ch. 3.1). Angle-closure glaucoma is usually initially approached by
laser iridotomy or peripheral iridectomy. Primary congenital glaucoma is usually treated
with surgery, likely trabeculotomy or goniotomy, or combinations of filtration surgery with
antifibrotic agents.
For repeated surgery, cyclodestructive procedures and tube implants are more commonly
used (See FC VI).
3.6.2 Techniques
Since glaucoma surgery is successfully practiced in different ways by different

ophthalmologists, a detailed description of surgical techniques is not within the scope
of this text.
The primary goal of surgery is to achieve a Target IOP without additional medication.
Additional medications can be used if a Target IOP is not reached by surgery alone.
Success rates of a surgical method in terms of IOP lowering can be best evaluated
in the absence of adjunctive medical treatment. The number of preoperative versus
postoperative medications may also depend on the variable compliance of the individual
patient before and after surgery. Also, it is useful to count the percentage of “successes”
below a defined IOP level as in Fig. 3.3. It is also important to consider not just the IOP
but complications rates and, most importantly, functional outcomes.
169
3.6.2.1 Penetrating Glaucoma Surgery
3.6.2.1.1 Trabeculectomy
The most widely used surgical procedure in OAG is the trabeculectomy, which produces
a ‘guarded’ fistula between the anterior chamber and the subconjunctival space178,179. The
introduction of improved operating microscopes, instruments and suture materials, has
led to numerous modifications and refinements of the original operation180. Modifications
include the size, shape and thickness of the scleral flap, limbal or fornix based
conjunctival flaps, fixed, releasable or adjustable sutures and the use of antimetabolites
and other antiscarring agents delivered in different ways to reduce wound healing181,182.
In the hands of experts the long-term success rate of filtering surgery alone, or with
adjunctive medical therapy in a previously unoperated eye has been reported at up
to 90%178; there are large differences however in the criteria used for the definition of
success and in the final success rates observed 183-192.
The use of stainless steel implants as facilitators for performing filtration surgery should
be weighted against the cost of the devices193-196.
Long-term IOP control is achieved in many cases, although some patients do require
further therapy or repeat surgery178,197,198.
The alternatives to trabeculectomy in OAG include non-penetrating surgeries and
drainage devices196,199-205.
Indications: [II,D]
1. In cases where other forms of therapy, like medicines or laser, have failed.
2. In cases where other forms of therapy are not suitable (e.g. where compliance
or side-effects are a problem) or appropriate medical treatment is not available.
3. In cases where a Target Pressure is required to prevent clinically significant
disease progression that cannot be reached with topical medications and/or
laser.
4. In cases which have such advanced glaucoma and high IOP at presentation that
other forms of treatment are unlikely to be successful.
Some studies have indicated that in terms of field survival, primary trabeculectomy was
superior to medical treatment, but these studies may not be relevant to current medical
practice as the evaluation of visual field was not done using todays analyses, and the
medical treatment options were very limited206. More recent studies suggest that visual
field progression is not significantly different whether initial treatment is medication or
trabeculectomy207, 208.
The ophthalmologist must assess the risks and benefits of early surgery in each
individual case.
Long-term risks of trabeculectomy:

Accelerated progression of senile cataracts is frequently seen after filtration surgery209,210.
Patients undergoing trabeculectomy should be advised on the symptoms of a developing
blebitis/endophthalmitis including red eye, tearing, discharge or decreased vision, and
should be warned to immediately seek the help of an ophthalmologist if any of these
170
symptoms develop in the operated eye211 [I,D]. Endophthalmitis is more common if

the bleb is thin and cystic - a situation more commonly found with the use of a small
treatment area of antimetabolites or full thickness filtration procedures. A long-tube
drainage device should be used if the bleb cannot be sited beneath the upper lid [I,D].
3.6.2.1.2 Trabeculotomy
Trabeculotomy, alone or combined with trabeculectomy, is generally used for congenital

and paediatric glaucoma and is less effective in adults212-214 [I,B]. It also may decrease
the need for further filtering and shunting procedures215.
A novel glaucoma procedure of trabeculotomy by internal approach was recently
introduced183,216,217.
3.6.2.2 Non-Penetrating Glaucoma Surgery
3.6.2.2.1 Deep Sclerectomy
In this technique, a deep lamella of corneosclera underneath the scleral flap is excised
thus removing the outer wall of Schlemm’s canal. The outer layer of the inner wall of
Schlemm’s canal is frequently also removed. Percolation of aqueous occurs through
the porosity of the remaining trabecular meshwork, possibly through micro-perforations.
When the scleral flap is repositioned, a “scleral lake” is created. A collagen implant or a
hyaluronic acid device is often used to keep this scleral lake open. In a number of cases,
a filtration bleb forms; long-term IOP levels appear higher than with trabeculectomy218-228.
3.6.2.2.2 Viscocanalostomy
In this technique, hyaluronic acid is injected into Schlemm’s canal in addition to the
dissection and excision of a deep lamella. The mechanism claimed to increase the
outflow is the widening of Schlemm’s canal and of the collector channels as well as
diffusion of aqueous from the “scleral lake”186,229,230.
The majority of randomised controlled trials suggests that the pressure lowering of
non-penetrating glaucoma surgery is not as marked as with trabeculectomy231-234.
3.6.2.2.3 Canaloplasty
Canaloplasty is a non-penetrating, bleb-independent, glaucoma surgery that combines a

2-flap dissection to the trabeculo-Descemet’s membrane, like in viscocanalostomy methods,
with a circumferential catheterization and viscodilation of Schlemm’s canal. In addition, a
10-0 polypropylene suture is placed within the canal to tension the inner wall and the
associated trabecular meshwork with the intention of preventing the Schlemm’s canal
collapse thus in theory restoring natural trabeculocanalicular aqueous outflow229,235-238.
171
This technique is indicated in POAG, pigmentary glaucoma and pseudoexfoliative

glaucoma and permits combined procedures with cataract surgery [II,D].
Contraindications to canaloplasty are primary or secondary ACG, neovascular glaucoma
or cases needing a low target IOP.
Intraoperative or postoperative complications (hyphema, hypotony secondary to a break
in the trabeculo-descemetic window, hypertension, cataract, endophthalmitis) have a
lower incidence than trabeculectomy239-242.
Arguments in favour of non-penetrating glaucoma surgery:

% minimal postoperative care (no bleb management)
% reduced incidence of hypotony-related complications and cataract
% reduced incidence of intraoperative complications (iris prolapse, expulsive
haemorrhage)
Arguments against non-penetrating glaucoma surgery:

% less efficient in IOP reduction (mean IOP 2-4 mmHg higher) than after
trabeculectomy
% difficult technique (learning curve)
% Nd:YAG laser goniopuncture often needed for IOP control
% Anatomical unpredictability
Arguments in favour of trabeculectomy:
% lower long-term postoperative IOP
% fewer lOP-lowering medications needed postoperatively
Arguments against trabeculectomy:
% possible higher rate of cataract formation
% postoperative bleb complications
% higher risk of postoperative hypotony and related complications (choroidal
detachment)
172
3.6.3 Methods of Preventing Filtering Bleb Scarring
3.6.3.1 Antimetabolites
Wound healing is one of the main determinants of the long-term intraocular pressure
control after filtering surgery 243,244. Excessive wound healing or repair leads to scar
formation in the conjunctiva. Risk factors for conjunctival scarring are young age, afro-
caribbean/hispanic race, inflammatory eye disease (e.g. uveitis, ocular pemphigoid,
Stevens-Johnson syndrome), long-term multiple topical medical therapy, aphakia by
intracapsular surgery, recent intraocular surgery (<3 months), previous conjunctival
incisional surgery, previous failed glaucoma filtration surgery, neovascular glaucoma188,245.
Antimetabolites such as 5-fluorouracil (5-FU) and mitomycin-C (MMC) are frequently
used in patients undergoing glaucoma filtration surgery in order to reduce postoperative
conjunctival scarring and improve drainage [I,A].
The use of these substances continues to be refined. Indications and techniques need
to be carefully considered, particularly the use of larger antimetabolite treatment areas
to minimise thin cystic blebs246,247 [I,D].
The risk of corneal epithelial erosions, epitheliopathy, late hypotony, bleb leaks, and
blebitis/endophthalmitis must be considered [I,D]. The use of antimetabolites, especially
MMC, is potentially hazardous, and requires careful surgical technique to prevent over
drainage and hypotony, or a thin focal drainage bleb with a higher risk of infection [I,D].
New antifibrotic agents and techniques are under investigation to more specifically
target and modulate the biological processes of wound healing after filtration surgery,
aiming for a lower risk of complications243,248-250.
3.6.3.1.1 General Precautions
The use of antimetabolites will enhance the unfavourable effect of any imprecision
during surgery. It is important to assess each individual case for risk factors, and/or
for the need of low target IOP and titrate the substance and dosage used accordingly
based on local experience.
If aqueous flow is not well controlled persistent hypotony will occur. Strategies to
increase control of flow include smaller sclerostomies, larger and/or thicker scleral flaps,
tighter suturing of the scleral flap, and releasable or adjustable sutures [II,D].
Research studies suggest that a large surface area of cytotoxic treatment together with
large scleral flaps and accurately sutured fornix-based conjunctival flaps lead to more
diffuse, posteriorly extended non-cystic blebs giving a considerable reduction in bleb-
related complications such as blebitis and endophthalmitis197,247,251,252 [I,B].
It is advisable for a surgeon not familiar with these drugs to start with weaker agents
(e.g. 5-FU rather than MMC) or lower concentrations of MMC [II,D].
Antimetabolites should not enter the eye [I,D]. 5-FU has a pH of 9.0 and one drop (0.05
ml) of MMC is enough to cause irreversible endothelial damage: precautions for use and
disposal of cytotoxic substances should be observed [I,D].
5-FU and MMC are not officially approved for ocular applications. Their use in many
cases as adjunctive in filtration surgery, however, has become standard clinical practice.
173
3.6.3.1.2 Administration
5-Fluorouracil:
% Intraoperative use [II,D]
Concentration: 25 or 50 mg/ml undiluted solution.
Administration: intraoperatively on a filter paper or a sponge.
Time of exposure: usually 5 minutes (shorter time has minimal effect).
Rinse: with at least 20 ml of balanced salt solution.
% Postoperative use [II,D]

Relative contraindication if epithelial problems present.
Concentration: 0.1 ml injection of 50 mg/ml undiluted solution.
Administration: adjacent to but not into bleb (pH 9), with a small calibre needle (e.g. 30
G needle on insulin syringe). Reflux from the injection site over the ocular surface should
be prevented253. Repeated injections are often necessary.
Mitomycin C:
% Intraoperative use [II,D]
Concentration: 0.1-0.5 mg/ml (care must be taken in diluting it to the desired
concentration).
Administration: intraoperatively on a filter paper or a sponge. Avoid contact with cut
edge of conjunctive flap.
Time of exposure: 1-5 minutes.
Rinse: with at least 20 ml of balanced salt solution.
% Postoperative use [II,D]

Concentration: 0.1 ml injection of 0.02 mg/ml solution.
Administration: adjacent to but not into bleb, with a small calibre needle (e.g. 30 G
needle on insulin syringe). Reflux from the injection site over the ocular surface should
be prevented253. A very small amount of MMC entering the eye will irreversibly damage
the endothelium. It is useful for some needling procedures but recommended only in
experienced hands.
3.6.3.2 Alternative Methods of Preventing Filtering Bleb Scarring
Irradiation, PDT and inhibition of growth factors have been used, but no long-term
clinical studies to support their use are yet available243,249.
Alternative Glaucoma Surgery

New alternative surgical techniques with the aim obtaining a higher safety profile than
filtration surgery were proposed during the last several years. Under the acronym
of M.I.G.S. “Minimally Invasive Glaucoma Surgery” are now collectively grouped
both ab-interno and ab-externo procedures, not necessarily involving the use of an
implantable device, not always bleb-independent for efficacy. The general aim would
be to entail significantly less tissue manipulation than filtration surgery, with less side
effects and sizeable IOP-lowering efficacy. There are no well controlled comparative
174
trials available to support the superiority among any of these procedures nor versus
trabeculectomy, for both safety and efficacy 254,255. These techniques are currently
performed in selected glaucoma patients with early to moderate disease and preferably
in combination with cataract surgery [II,D].
ALTERNATIVE GLAUCOMA SURGERY (*)

Based on subconjunctival filtration
- trans-scleral filtration, ab-interno device (AqueSys Xen)
- trans-scleral filtration, ab-externo device (InnFocus Microshunt)
Based on suprachoroidal drainage
- suprachoroidal stents, ab-interno (Glaukos iStent Supra, Transcend CyPass)
Based on Schlemm’s canal drainage/bypass/expansion
- trabecular bypass stents/canal expanders (Glaukos iStent, Ivantis Hydrus)
- ab-Interno trabeculectomy (Trabectome)
- ab-externo canaloplasty/trabeculotomy (iScience catheter)
(*) THIS LIST IS NOT ALL INCLUSIVE. The EGS does not endorse any product or
procedures.
3.6.4 Complex Cases
Complicated glaucoma cases such as those that have failed previous surgery, secondary
glaucomas, congenital glaucomas, et cetera require specialist treatment. In addition to
trabeculectomy, other forms of therapy may be necessary such as drainage devices
and ciliary body ablation.
3.6.5 Long-Tube Drainage Devices
The use of long-tube drainage devices such as those described by Molteno256-263,

Krupin 26 4-26 6 , Baer veldt 267-272 , A hmed 26 8, 273 -28 0 or Schocket 281-28 4 are generally
reserved for patients with risk factors for a poor result with trabeculectomy with
antimetabolite [II,D], although recent trials established their efficacy and safety as a
primary surgical procedure258,285 [II,B].
Factors that decrease the chances of successful trabeculectomies and, therefore, make
tube surgery attractive, include previous failed filtering surgery with antimetabolites,
excessive conjunctival scarring due to previous ocular surgery with severe conjunctival
or surface disease, active neovascular disease, paediatric aphakia, or where filtration
surgery is going to be technically difficult286,287 [II,D].
175
3.7 - CATARACT AND GLAUCOMA SURGERY

When glaucoma surgery is indicated and there is a visually significant cataract the two
procedures can be performed combined or sequentially. The decision is to be made
according to the clinical findings, after discussing with the patients advantages and
disadvantages of each approach [I,D].
In case of angle closure or narrow angle approach, it is important to evaluate the lens
as a component of the raised IOP [I,D] (See also Ch 2.4)
Small-incision phacoemulsification cataract extraction is one of the most relevant
surgical advances for our glaucoma patients. It allows faster and better visual recovery,
and with appropriate techniques it is safely applicable in cases with small pupil, shallow
AC or pre-existing filtering blebs. Futhermore it can be combined effectively and safely
with filtering procedures, including trabeculectomy, miniature drainage implants and
deep sclerectomy205,288-290.
Dif ferent new glaucoma surgical techniques which can be combined with
phacoemulsification (i.e endoscopic cyclophotocoagulation, trabecular bypass stents,
ab interno trabeculectomy and canaloplasty) have been proposed in the last years291.
Randomized clinical trials are presently needed to clarify this topic.
Despite the improved results of small incision phacoemulsification and of filtration
surgery with anti-metabolites there is no evidence to support a generalized switch from
sequential to combined surgery and viceversa [I,D].
In summary:
% Modern phacoemulsification with clear cornea incisions does not interfere with
subsequent glaucoma surgical procedures292
% The development or worsening of a visually significant cataract is common after
glaucoma surgery209
% Cataract surgery performed after trabeculectomy can affect the IOP control209,293
% Cataract surgery alone may be of limited benefit in lowering the IOP in open
angle glaucoma and the effect appears to be proportional to the preoperative IOP
values; such effect may be greater in angle closure glaucoma / narrow angles and
appears to be proportional to the degree of anterior chamber opening294-296
% Combined procedures allow for greater IOP reduction and fewer IOP spikes in the
immediate postoperative period than phacoemulsification alone297-299
% The success rate of combined phacoemulsification and filtration surgery is usually
not as favourable as filtration surgery alone and the use of antimetabolites is
recommended in all cases.
176
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284. Spiegel D, Shrader RR, Wilson RP. Anterior chamber tube shunt to an encircling
band (Schocket procedure) in the treatment of refractory glaucoma. Ophthalmic Surg
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286. Schmidt W, Kastner C, Sternberg K, et al. New concepts for glaucoma implants--
controlled aqueous humor drainage, encapsulation prevention and local drug delivery. Curr
Pharm Biotechnol 2013;14(1):98-111.
287. Patel S, Pasquale LR. Glaucoma drainage devices: a review of the past, present, and
future. Semin Ophthalmol 2010;25(5-6):265-70.
288. Kanner EM, Netland PA, Sarkisian SR, Jr., Du H. Ex-PRESS miniature glaucoma device
implanted under a scleral flap alone or combined with phacoemulsification cataract
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289. Tzu JH, Shah CT, Galor A, et al. Refractive Outcomes of Combined Cataract and
Glaucoma Surgery. J Glaucoma 2013.
290. Bilgin G, Karakurt A, Saricaoglu MS. Combined non-penetrating deep sclerectomy with
phacoemulsification versus non-penetrating deep sclerectomy alone. Semin Ophthalmol
2014;29(3):146-50.
291. Budenz DL, Gedde SJ. New options for combined cataract and glaucoma surgery. Curr
Opin Ophthalmol 2014;25(2):141-7.
292. Netland PA. Cataract surgery in glaucoma patients: how much benefit? Am J Ophthalmol
2014;157(1):1-3.
293. Nguyen DQ, Niyadurupola N, Tapp RJ, et al. Effect of phacoemulsification on trabeculectomy
function. Clin Experiment Ophthalmol 2013.
294. Vizzeri G, Weinreb RN. Cataract surgery and glaucoma. Curr Opin Ophthalmol
2010;21(1):20-4.
295. Slabaugh MA, Chen PP. The effect of cataract extraction on intraocular pressure. Curr
Opin Ophthalmol 2014;25(2):122-6.
296. Slabaugh MA, Bojikian KD, Moore DB, Chen PP. The effect of phacoemulsification
on intraocular pressure in medically controlled open-angle glaucoma patients. Am J
Ophthalmol 2014;157(1):26-31.
297. Shingleton BJ, Wooler KB, Bourne CI, O’Donoghue MW. Combined cataract and
trabeculectomy surgery in eyes with pseudoexfoliation glaucoma. J Cataract Refract Surg
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298. Marchini G, Ceruti P, Vizzari G. Management of concomitant cataract and glaucoma. Dev
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299. Liaska A, Papaconstantinou D, Georgalas I, et al. Phaco-Trabeculectomy in Controlled,
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191
INDEX
CDR ∙ 27, 54, 76
5 Central Corneal Thickness ∙ 27, 33, 35, 80, 83, 85, 136
5-Fluorouracil ∙ 18, 27, 173-174 Childhood Glaucomas ∙ 75-76
5-FU ∙ 27, 173 Chronic Angle-Closure Glaucoma ∙ 27, 105, 111, 139
CIGTS ∙ 16, 18, 27, 82-83
A Ciliary band ∙ 40
Acetozolamide ∙ 148 Ciliary block ∙ 117
Acute Angle-Closure ∙ 27, 40, 100, 102-103, 105- Ciliary body cysts ∙ 118
106, 109-110, 112, 114, 119 Clonidine ∙ 149, 164
Adherence ∙ 21, 138, 159-160, 164 CNTGS ∙ 15, 27, 82-83
Adrenergic Agonists ∙ 140, 149-151 Colour coded map ∙ 60
AGIS ∙ 16, 18-19, 27, 82-83 Combination Therapy ∙ 85, 141-142, 158
Alpha zone ∙ 51 Compliance ∙ 12, 21, 89, 139-140, 158-159, 169-
ALT ∙ 16, 19, 27, 92, 95, 116, 164-165 170
Aniridia ∙ 77, 116, 119, 168 Congenital anomalies ∙ 59, 79, 84, 119
Antiglaucoma Drugs ∙ 139, 145 Congenital glaucoma ∙ 28, 75-76, 88, 155, 169, 175
Antimetabolites ∙ 85, 87, 115, 117, 170-171, 173, 175-176 Corticosteroid treatment ∙ 97
Apraclonidine ∙ 149, 164 Cost-Effectiveness ∙ 20
Aqueous misdirection ∙ 104, 108, 112, 117 Cup/Disc ratio ∙ 27, 54, 83
Argon laser iridotomy ∙ 107, 162 Cyclophotocoagulation ∙ 98, 167-168, 176
Argon Laser Peripheral Iridoplasty ∙ 27, 105-106,
108, 110 D
Assessing progression ∙ 63 DCT ∙ 27, 34, 38
Deep Sclerectomy ∙ 171, 176
B Diabetes ∙ 28, 81, 97-98, 103, 147
Bebié curve ∙ 61 Dichlorphenamide ∙ 148
Befunolol ∙ 147 Dietary Supplementation ∙ 153
Beta zone ∙ 51 Dipivefrin ∙ 145, 150
Beta-Receptor Antagonists ∙ 147 Direct Gonioscopy ∙ 41, 44
Betaxolol ∙ 15, 147, 155 Disc diameter ∙ 50, 53
Bimatoprost ∙ 142, 145-146, 151 Disc haemorrhages ∙ 16-17, 19, 48, 50, 83, 85
Bleb Scarring ∙ 173-174 Diurnal variations ∙ 33
Blindness ∙ 21, 79, 102, 131-132, 135 Dorzolamide ∙ 17, 142, 145, 148
Breast-feeding ∙ 153, 155-156 Dynamic contour tonometry ∙ 27, 33-34
Brimonidine ∙ 133, 141-142, 145, 149, 155-156, 164 Dynamic indentation gonioscopy ∙ 42-43
Brinzolamide ∙ 141-142, 145, 148 Dynamic Strategy ∙ 58
C E
Canaloplasty ∙ 171-172, 175-176 EGPS ∙ 17, 27, 81-82
Carbachol ∙ 110, 150 EMGT ∙ 15, 19, 27, 63, 82-83
Carbonic Anhydrase Inhibitors ∙ 94, 107, 140, 145, Epidemiology ∙ 75, 79, 91-92
148, 151, 155-156 Epinephrine ∙ 145, 150
Carteolol ∙ 142, 147 Episcleral Venous Pressure ∙ 99
Cataract ∙ 15, 17-19, 77-78, 90-91, 93, 96, 98, 101, Ethnicity ∙ 80
104, 108-109, 113-114, 117, 168, 170, 172, 175-176 Event analyses ∙ 63
CCT ∙ 16-17, 19, 27, 33, 35, 80-83, 85, 135 Exfoliative glaucoma ∙ 29, 90
192
Intermittent Angle-Closure ∙ 28, 85, 88, 105, 110
F Intraocular pressure ∙ 11, 17, 19-20, 28, 33-35,
False negative answers ∙ 27, 60 38, 80, 83-84, 101, 103, 110, 134, 145, 158,
False positive answers ∙ 27, 60, 62 167, 173
Family history ∙ 13, 14, 80, 82-83, 97, 104 Intraocular tumour ∙ 95
FDT ∙ 27, 59 IOP ∙ 11-19, 28, 33-35, 37, 38, 44, 75-76, 78,
First Line Drugs ∙ 146, 151 80-96, 98-109, 112-116, 118-119, 132-138, 140-
Fixation losses ∙ 27, 60 153, 156, 158, 160-161, 163-166, 169-174, 176
Fixed Combination therapy ∙ 141, 158 Iridocorneal endothelial syndrome ∙ 115
FL ∙ 27, 60 Iridotomy ∙ 28, 44, 92, 100, 102-108, 110-114, 117,
Flicker perimetry ∙ 59 119, 150, 161-163, 166, 169
FN ∙ 27, 60 Iris processes ∙ 40
FP ∙ 27, 59-61 Iris root ∙ 40, 45, 98
Frequency Doubling Technology ∙ 27, 59 ISNT rule ∙ 48, 52
G J
Gaze tracker ∙ 60 Juvenile Glaucoma ∙ 86, 88
GHT ∙ 27, 61
Glaucoma Hemifield Test ∙ 27, 61 L
Goal of glaucoma treatment ∙ 12, 132 Laser Iridoplasty ∙ 103, 108, 110
Goldmann applanation tonometry ∙ 27, 33, 35-36, 38 Laser Iridotomy ∙ 44, 106-107, 110-111, 114, 119,
Goldmann perimetry ∙ 58 161-162, 169
Gonioscopy ∙ 14, 39-45, 47, 76, 85-86, 88, 92, 96, Laser Trabeculoplasty ∙ 15, 18, 85-88, 91-92,
100-101, 106, 112-113, 163-164 97-98, 112, 116, 137, 155, 164-166
Goniotomy ∙ 76, 78, 88, 169 Latanoprost ∙ 142, 145-146, 151, 153
Grey scale ∙ 60 Llearning effect ∙ 62
GSS ∙ 27, 61, 64 Lens-induced open-angle glaucoma ∙ 93
Levobunolol ∙ 147
H LV ∙ 61, 63
Heidelberg Edge Perimetry ∙ 27, 59
Heidelberg Retina Tomography ∙ 27, 56 M
HEP ∙ 27, 59 Malignant glaucoma ∙ 100, 109, 117
High Pressure Glaucoma ∙ 27, 84 Manual kinetic perimetry ∙ 58
High-pass resolution perimetry ∙ 27, 59 MD ∙ 16, 18-19, 61, 63-64, 132
Hodapp Classification ∙ 64 Mean defect ∙ 61
HRP ∙ 27, 59 Methozolamide ∙ 148
HRT ∙ 27, 56 Metipranolol ∙ 142, 147
Humphrey Field Analyzer ∙ 59 Migraine ∙ 81
Humphrey Perimeter ∙ 58, 61 Mission statement ∙ 12
Mitomycin C ∙ 173-174
I MMC ∙ 173-174
Icare ∙ 33, 35, 38 Monotherapy ∙ 140-141, 145, 158
Imaging ∙ 47, 55-56, 57 Myopia ∙ 40, 80-81, 97, 148, 150
Incisional surgery ∙ 84, 139, 142, 169, 173
Indirect Gonioscopy ∙ 41, 44 N
Individualized glaucoma treatment ∙ 133 NCT ∙ 34, 38
193
Neovascular Glaucoma ∙ 95, 115, 119, 150, 168, 173 Primary Angle-closure Glaucoma ∙ 100-101
Neuroprotection ∙ 12, 84, 133, 156 Primary Angle-closure Suspect ∙ 101, 105
Neuroretinal Rim ∙ 48, 51-52 Primary congenital glaucoma ∙ 75-76, 169
Non-contact tonometry ∙ 34 Primary Juvenile Glaucoma ∙ 86
Non-Penetrating Glaucoma Surgery ∙ 171-172 Primary Open-Angle Glaucoma ∙ 16, 79, 83-85,
Normal-Pressure Glaucoma ∙ 85 87-88, 100
Numerical pattern deviation map ∙ 60 Primary Open-Angle Glaucoma Suspect ∙ 87
Numerical threshold map ∙ 60 Primary Open-Angle Glaucomas ∙ 79
Numerical total deviation map ∙ 60 Probability maps ∙ 60-61, 63
Progression rate ∙ 14-16, 132-133
O Prostaglandin Analogues ∙ 95, 141, 146, 151, 155,
Octopus perimeter ∙ 67 165
Ocular Hypertension ∙ 16, 18-21, 79, 81-83, 88-89, Provocative Tests ∙ 100
92-93, 98, 133, 164 PSD ∙ 17, 61, 64, 81
Ocular perfusion pressure ∙ 81 Pseudoexfoliation ∙ 15, 17, 19, 39-40, 79-80, 82, 90
Ocular Response Analyser ∙ 34 Pseudoexfoliation glaucoma ∙ 15
Ocular trauma ∙ 13, 96 Pupillary block ∙ 42-43, 91-94, 102-103, 105-111,
Ocuton ∙ 34, 38 113-115, 117, 161
OHTS ∙ 16, 14, 19, 81-82
Optic disc ∙ 15-18, 48-56, 83, 85-88, 110, 140 Q
Optic disc haemorrhage ∙ 50, 83 Quality of life ∙ 12-13, 18, 75, 78, 119, 131-132, 134,
Optic disc size ∙ 53, 54 138, 140
ORA ∙ 34, 38
Osmotics ∙ 106-108, 117, 145, 151 R
Race ∙ 80, 104
P Randomized glaucoma trials ∙ 15
Parapapillary atrophy ∙ 51 Rate of Progression ∙ 12, 14, 17, 19, 55, 63, 86,
Parasympathomimetics ∙ 104, 107, 150 131-136, 138
Pascal ∙ 34 Raynaud syndrome ∙ 81
Pediatric glaucoma ∙ 76 Rebound tonometry ∙ 35
Penetrating Glaucoma Surgery ∙ 170-172 Reliability indices ∙ 60
Perfusion pressure ∙ 81, 133 Retinal detachment ∙ 96, 150
Perimetry ∙ 16, 58-59, 62-63 Retinal nerve Fibre layer ∙ 48, 50, 55-56, 79, 84, 88
Persistence ∙ 12, 159-160 Retinopathy of prematurity ∙ 77, 118
Phacolytic glaucoma ∙ 91-92, 111 Rim Width ∙ 54
Pigmentary glaucoma ∙ 164, 172 Ring perimetry ∙ 59
Pilocarpine ∙ 87, 92, 95, 103, 107, 110-111, 113, Risk factors ∙ 13, 79-81, 83-84, 87-89, 97-98, 104,
142, 145, 150, 161, 166 115-116, 132-136, 146, 173, 175
Plateau iris ∙ 103, 105, 108-110, 113, 166 RNFL ∙ 48, 50, 86-87, 89
Pneumatonometry ∙ 34 RoP ∙ 14, 131-132
Posterior polymorphous dystrophy ∙ 77, 116
Pregnancy ∙ 153-156, 158 S
Preservatives ∙ 141, 152 SAP ∙ 58-59, 63
Primary angle-closure glaucoma ∙ 100 Scanning laser polarimetry ∙ 56
Primary Angle-Closure Suspect ∙ 101, 105 Schlemm's canal ∙ 40, 76, 171, 175
Primary Angle-Closure ∙ 83, 100-105, 110, 115 Schwalbe's line ∙ 40, 45, 91, 92, 106
194
Scleral spur ∙ 40, 45, 150 Uveal effusion ∙ 100, 118, 127
Secondary Angle-Closure ∙ 94, 104-105, 108, Uveitic glaucoma ∙ 94-95
114-115, 117
Secondary Angle-Closure With Pupillary Block ∙ 114 V
Secondary Childhood Glaucoma ∙ 76-78 Van Herick grading ∙ 47
Secondary Glaucomas ∙ 90, 100, 175 VFI ∙ 61, 63, 132
Secondary Open-Angle Glaucoma ∙ 90, 97, 99 Viscocanalostomy ∙ 171
Selective Adrenergic Agonists ∙ 149-151 Visual field indices ∙ 60-61, 79
Short Wavelength Automated Perimetry ∙ 59 Visual field testing ∙ 55-56, 58
Silicon oil ∙ 96, 98, 118
SITA Fas ∙ 58 Y
SITA Standard ∙ 58 YAG laser iridotomy ∙ 107, 114, 161
Sleep apnoea ∙ 81
SLT ∙ 95, 164-165
Spaeth Grading System ∙ 45
Staging ∙ 62, 64, 101, 110
Standard Automated Perimetry ∙ 58
Static computerised perimetry ∙ 58
Strength of recommendation ∙ 11
Sturge-Weber syndrome ∙ 77, 99, 119
SWAP ∙ 59
T
Tafluprost ∙ 141-142, 145, 151
Target IOP ∙ 11-12, 14, 18, 83, 86, 91, 134-138,
140, 169, 172-173
Test point patterns ∙ 58-59
Timolol ∙ 141-142, 145, 147, 155-157
Tonometers ∙ 33-34, 38, 75
Tonometry ∙ 34-36, 38, 44, 132
Tono-Pen ∙ 35
TOP algorithm ∙ 58
Topical Medications ∙ 137, 142, 152, 170
Trabecular Meshwork ∙ 40, 75, 84, 90-96, 98,
101-103, 105, 109, 115-116, 150, 163-165, 171
Trabeculectomy ∙ 18-19, 102, 104, 106, 109,
170-172, 175-176
Trabeculotomy ∙ 76, 78, 87-88, 116, 169, 171, 175
Transpalpebral tonometry ∙ 35
Travoprost ∙ 142, 146, 151
Trend analyses ∙ 63
Triggerfish ∙ 35
Tube Drainage Devices ∙ 175
U
UGH syndrome ∙ 98
195

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Copyright © 2014 European Glaucoma Society

CHAPTER 1 - PATIENT EXAMINATION 31

1.1 Intraocular pressure (iop) and tonometry 33

CHAPTER 2 - CLASSIFICATION AND TERMINOLOGY 73

2.1 Primary congenital forms/childhood glaucomas 75

CHAPTER 3 - TREATMENT PRINCIPLES AND OPTIONS 129

3.1 General Principles of Glaucoma Treatment 131

Glaucoma is a living specialty, with new ideas on causation, mechanisms and

The Guidelines Writers The Guidelines The EGS Committees

For Conflict of interest/Financial disclosure please see www.eugs.org/pdf/FinancialDisclosure.pdf

Clinical care must be individualised to the patient, the treating ophthalmologist

I.1 Terminology, Classification and Definitions

1. Anatomy / Structure (See Ch. 1)

I.2 Treatment Principles

A. Treatment Goals (See Ch. 3.1)

B. Suggested ways of reaching the goal (see Ch. 3 and 4)

B.3. Incorporation of a quality of life measure in the outcome of treatment

• prevention of visual disability in those at risk of decreased quality of life;

FC I – Suggested Questions for Your

© European Glaucoma Society 2014

Evaluation of Functional Loss / Time for Individualized Treatment

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Figure 1. Evaluation of functional loss/time for individualised treatment

The EGS guidelines are to be adapted to individual patients, socioeconomic

II - RANDOMIZED CONTROLLED TRIALS FOR GLAUCOMA

II.1 Treatment Vs No Treatment Trials

II.1.1 Collaborative Normal Tension Glaucoma Study (CNTGS)

CNTGS compared treatment versus no treatment in normal tension glaucoma. Eligible

II.1.2 Early Manifest Glaucoma Trial (EMGT)

EMGT was a randomized, prospective trial comparing treatment versus no treatment

II.1.3 The Ocular Hypertension Treatment Study (OHTS)

II.1.4 European Glaucoma Prevention Study (EGPS)

The EGPS was a multicentre, randomized, double-masked, placebo-controlled clinical

II.2 Studies Comparing Treatments

II.2.1 Collaborative Initial Glaucoma Treatment Study (CIGTS)

II.2.2 Advanced Glaucoma Intervention Study (AGIS)

III - COST-EFFECTIVENESS OF GLAUCOMA CARE

III.1 Case Detection And Screening for Glaucoma

No randomized screening, diagnostic and follow-up trials reporting the clinical

III.3 Treatment of Glaucoma and Ocular Hypertension in Preventing Visual

III.4 Follow-Up Protocols And Models Of Care

1. Group CN-TGS. Comparison of glaucomatous progression between untreated patients with

Ann Intern Med 2013;158(4):271-9.

HSV Herpes Simplex Virus

POAG Primary Open-Angle Glaucoma

1.1 - INTRAOCULAR PRESSURE (IOP) AND TONOMETRY

1.1.1 Methods of measurement (tonometry)

1.1.1.1 Goldmann applanation tonometry (GAT)

1.1.1.2 Alternative tonometers (in alphabetical order):

% Dynamic contour tonometry (DCT, or Pascal)

% Non-contact tonometry (NCT)

% Ocular Response Analyser (ORA)

% Rebound tonometry (Icare)

% Triggerfish® (Sensimed) has a sensor embedded in a contact lens, based on strain

1.1.2 Intraocular pressure and central corneal thickness

Except for unusual circumstances, there is no evidence to support the use

Technique of Goldmann Applanation Tonometry.

© European Glaucoma Society 2014

Reading on dial Higher than IOP Lower than IOP

Centration correct correct incorrect

© European Glaucoma Society 2014

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